A 59‐year‐old man presented to the emergency department with the acute onset of right‐sided abdominal and flank pain. The pain had begun the previous night, was constant and progressively worsening, and radiated to his right groin. He denied fever, nausea, emesis, or change in his bowel habits, but he did notice mild right lower quadrant discomfort with micturition. Upon further questioning, he also complained of mild dyspnea on climbing stairs and an unspecified recent weight loss.

The most common cause of acute severe right‐sided flank and abdominal pain radiating to the groin and associated with dysuria in a middle‐aged man is ureteral colic. Other etiologies important to consider include retrocecal appendicitis, pyelonephritis, and, rarely, a dissecting abdominal aortic aneurysm. This patient's seemingly recent onset exertional dyspnea and weight loss do not neatly fit any of the above, however.

His past medical history was significant for diabetes mellitus and pemphigus vulgaris diagnosed 7 months previously. He had been treated with prednisone, and the dose decreased from 100 to 60 mg daily, 1 month previously, due to poor glycemic control as well as steroid‐induced neuropathy and myopathy. His other medications included naproxen sodium and ibuprofen for back pain, azathioprine, insulin, pioglitazone, and glimiperide. He had no past surgical history. He had lived in the United States since his emigration from Thailand in 1971. His last trip to Thailand was 5 years previously. He was a taxi cab driver. He had a ten‐pack year history of tobacco use, but had quit 20 years prior. He denied history of alcohol or intravenous drug use.

Pemphigus vulgaris is unlikely to be directly related to this patient's presentation, but in light of his poorly controlled diabetes, his azathioprine use, and particularly his high‐dose corticosteroids, he is certainly immunocompromised. Accordingly, a disseminated infection, either newly acquired or reactivated, merits consideration. His history of residence in, and subsequent travel to, Southeast Asia raises the possibility of several diseases, each of which may be protean in their manifestations; these include tuberculosis, melioidosis, and penicilliosis (infection with Penicillium marneffei). The first two may reactivate long after initial exposure, particularly with insults to the immune system. The same is probably true of penicilliosis, although I am not certain of this. On a slightly less exotic note, domestically acquired infection with histoplasmosis or other endemic fungi is possible.

On examination he was afebrile, had a pulse of 130 beats per minute and a blood pressure of 65/46 mmHg. His oxygen saturation was 92%. He appeared markedly cushingoid, and had mild pallor and generalized weakness. Cardiopulmonary examination was unremarkable. His abdominal exam was notable for distention and hypoactive bowel sounds, with tenderness and firmness to palpation on the right side. Peripheral pulses were normal. Examination of the skin demonstrated ecchymoses over the bilateral forearms, and several healed pemphigus lesions on the abdomen and upper extremities.

The patient's severely deranged hemodynamic parameters indicate either current or impending shock, and resuscitative measures should proceed in tandem with diagnostic efforts. The cause of his shock seems most likely to be either hypovolemic (abdominal wall or intra‐abdominal hemorrhage, or conceivably massive third spacing from an intra‐abdominal catastrophe), or distributive (sepsis, or acute adrenal insufficiency if he has missed recent steroid doses). His ecchymoses may simply reflect chronic glucocorticoid use, but also raise suspicion for a coagulopathy. Provided the patient can be stabilized to allow this, I would urgently obtain a computed tomography (CT) scan of the abdomen and pelvis.

Initial laboratory studies demonstrated a hemoglobin of 9.1 g/dL, white blood cell count 8000/L with 33% bands, 48% segmented neutrophils, 18% lymphocytes, and 0.7% eosinophils, platelet count 356,000/L, sodium 128 mmol/L, BUN 52 mg/dL, creatinine 2.3 mg/dL, and glucose of 232 mg/dL. Coagulation studies were normal, and lactic acid was 1.8 mmol/L (normal range, 0.7‐2.1). Fibrinogen was normal at 591 and LDH was mildly elevated at 654 (normal range, 313‐618 U/L). Total protein and albumin were 3.6 and 1.9 g/dL, respectively. Total bilirubin was 0.6 mg/dL. Random serum cortisol was 20.2 g/dL. Liver enzymes, amylase, lipase, iron stores, B₁₂, folate, and stool for occult blood were normal. Initial cardiac biomarkers were negative, but subsequent troponin‐I was 3.81 ng/mL (elevated, >1.00). Urinalysis showed 0‐4 white blood cells per high powered field.

The laboratory studies provide a variety of useful, albeit nonspecific, information. The high percentage of band forms on white blood cell differential further raises concern for an infectious process, although severe noninfectious stress can also cause this. While we do not know whether the patient's renal failure is acute, I suspect that it is, and may result from a variety of insults including sepsis, hypotension, and volume depletion. His moderately elevated troponin‐I likely reflects supplydemand mismatch or sepsis. I would like to see an electrocardiogram, and I remain very interested in obtaining abdominal imaging.

Chest radiography showed pulmonary vascular congestion without evidence of pneumothorax. Computed tomography scan of the abdomen and pelvis showed retroperitoneal fluid bilaterally (Figure 1). This was described as suspicious for ascites versus hemorrhage, but no obvious source of bleeding was identified. There was also a small amount of right perinephric fluid, but no evidence of a renal mass. The abdominal aorta was normal; there was no lymphadenopathy.

Figure 1

The CT image appears to speak against simple ascites, and seems most consistent with either blood or an infectious process. Consequently, the loculated right retroperitoneal collection should be aspirated, and fluid sent for fungal, acid‐fast, and modified acid‐fast (i.e., for Nocardia) stains and culture, in addition to Gram stain and routine aerobic and anaerobic cultures.

The patient was admitted to the intensive care unit. Stress‐dose steroids were administered, and he improved after resuscitation with fluid and blood. His renal function normalized. Urine and blood cultures returned negative. His hematocrit and multiple repeat CT scans of the abdomen remained stable. A retroperitoneal hemorrhage was diagnosed, and surgical intervention was deemed unnecessary. Both adenosine thallium stress test and echocardiogram were normal. He was continued on 60 mg prednisone daily and discharged home with outpatient follow‐up.

This degree of improvement with volume expansion (and steroids) suggests the patient was markedly volume depleted upon presentation. Although a formal adrenocorticotropic hormone (ACTH) stimulation test was apparently not performed, the random cortisol level suggests adrenal insufficiency was unlikely to have been primarily responsible. While retroperitoneal hemorrhage is possible, the loculated appearance of the collection suggests infection is more likely.

Three weeks later, he was readmitted with recurrent right‐sided abdominal and flank pain. His temperature was 101.3F, and he was tachycardic and hypotensive. His examination was similar to that at the time of his previous presentation. Laboratory data revealed white blood cell count of 13,100/L with 43% bands, hemoglobin of 9.2 g/dL, glucose of 343 mg/dL, bicarbonate 25 mmol/L, normal anion gap and renal function, and lactic acid of 4.5 mmol/L. Liver function tests were normal except for an albumin of 3.0 g/dL. CT scan of the abdomen revealed loculated retroperitoneal fluid collections, increased in size since the prior scan.

The patient is once again evidencing at least early shock, manifested in his deranged hemodynamics and elevated lactate level. I remain puzzled by the fact that he appeared to respond to fluids alone at the time of his initial hospital stay, unless adrenal insufficiency played a greater role than I suspected. Of note, acute adrenal insufficiency could explain much of the current picture, including fever, and bland (uninfected) hematomas are an underappreciated cause of both fever and leukocytosis. Having said this, I remain concerned that his retroperitoneal fluid collections represent abscesses. The most accessible of these should be sampled.

Aspiration of the retroperitoneal fluid yielded purulent material which grew Klebsiella pneumoniae. The cultures were negative for mycobacteria and fungus. Blood and urine cultures were negative. Drains were placed, and he was followed as an outpatient. His fever and leukocytosis subsided, and he completed a 6‐week course of trimethoprim‐sulfamethoxazole. CT imaging confirmed complete evacuation of the fluid.

Retroperitoneal abscesses frequently present in smoldering fashion, although patients may be quite ill by the time of presentation. Most of these are secondary, i.e., they arise from another abnormality in the retroperitoneum. Most commonly this is in the large bowel, kidney, pancreas, or spine. I would carefully scour his follow‐up imaging for additional clues and, if unrevealing, proceed to colonoscopy.

He returned 1 month after drain removal, with 2‐3 days of nausea and abdominal pain. His abdomen was moderately distended but nontender, and multiple persistent petechial and purpuric lesions were present on the upper back, chest, torso, and arms. Abdominal CT scan revealed small bowel obstruction and a collection of fluid in the left paracolic gutter extending into the left retrorenal space.

The patient does not appear to have obvious risk factors for developing a small bowel obstruction. No mention is made of the presence or absence of a transition point on the CT scan, and this should be ascertained. His left‐sided abdominal fluid collection is probably infectious in nature, and I continue to be suspicious of a large bowel (or distal small bowel) source, via either gut perforation or bacterial translocation. The collection needs to be percutaneously drained for both diagnostic and therapeutic reasons, and broadly cultured. Finally, we need to account for the described dermatologic manifestations. The purpuric/petechial lesions sound vasculitic rather than thrombocytopenic in origin based on location; conversely, they may simply reflect a corticosteroid‐related adverse effect. I would like to know whether the purpura was palpable, and to repeat a complete blood count with peripheral smear.

Laboratory data showed hemoglobin of 9.3 g/dL, a platelet count of 444,000/L, and normal coagulation studies. The purpura was nonpalpable (Figure 2). The patient had a nasogastric tube placed for decompression, with bilious drainage. His left retroperitoneal fluid was drained, with cultures yielding Enterococcus faecalis and Enterobacter cloacae. The patient was treated with a course of broad‐spectrum antibiotics. His obstruction improved and the retroperitoneal collection resolved on follow‐up imaging. However, 2 days later, he had recurrent pain; abdominal CT showed a recurrence of small bowel obstruction with an unequivocal transition point in the distal jejunum. A small fluid collection was noted in the left retroperitoneum with a trace of gas in it. He improved with nasogastric suction, his prednisone was tapered to 30 mg daily, and he was discharged home.

Figure 2

The isolation of both Enterococcus and Enterobacter species from his fluid collection, along with the previous isolation of Klebsiella, strongly suggest a bowel source for his recurrent abscesses. Based on this CT report, the patient has clear evidence of at least partial small bowel obstruction. He lacks a history of prior abdominal surgery or other more typical reasons for obstruction caused by extrinsic compression, such as hernia, although it is possible his recurrent abdominal infections may have led to obstruction due to scarring and adhesions. An intraluminal cause of obstruction also needs to be considered, with causes including malignancy (lymphoma, carcinoid, and adenocarcinoma), Crohn's disease, and infections including tuberculosis as well as parasites such as Taenia and Strongyloides. While the purpura is concerning, given the nonpalpable character along with a normal platelet count and coagulation studies, it may be reasonable to provisionally attribute it to high‐dose corticosteroid use.

He was admitted a fourth time a week after being discharged, with nausea, generalized weakness, and weight loss. At presentation, he had a blood pressure of 95/65 mmHg. His white blood cell count was 5,900/L, with 79% neutrophils and 20% bands. An AM cortisol was 18.8 /dL. He was thought to have adrenal insufficiency from steroid withdrawal, was treated with intravenous fluids and steroids, and discharged on a higher dose of prednisone at 60 mg daily. One week later, he again returned to the hospital with watery diarrhea, emesis, and generalized weakness. His blood pressure was 82/50 mmHg, and his abdomen appeared benign. He also had an erythematous rash over his mid‐abdomen. Laboratory data was significant for a sodium of 127 mmol/L, potassium of 3.0 mmol/L, chloride of 98 mmol/L, bicarbonate of 26 mmol/L, glucose of 40 mg/dL, lactate of 14 mmol/L, and albumin of 1.0 g/dL. Stool assay for Clostridium difficile was negative. A CT scan of the abdomen and pelvis showed small bilateral pleural effusions and small bowel fluid consistent with gastroenteritis, but without signs of obstruction. Esophagogastroduodenoscopy (EGD) showed bile backwash into the stomach, as well as inflammatory changes in the proximal and mid‐stomach, and inflammatory reaction and edema in the proximal duodenum. Colonoscopy showed normal appearing ileum and colon.

The patient's latest laboratory values appear to reflect his chronic illness and superimposed diarrhea. I am perplexed by his markedly elevated serum lactate value in association with a normal bicarbonate and low anion gap, and would repeat the lactate level to ensure this is not spurious. His hypoglycemia probably reflects a failure to adjust or discontinue his diabetic medications, although both hypoglycemia and type B lactic acidosis are occasionally manifestations of a paraneoplastic syndrome. The normal colonoscopy findings are helpful in exonerating the colon, provided the preparation was adequate. Presumably, the abnormal areas of the stomach and duodenum were biopsied; I remain suspicious that the answer may lie in the jejunum.

The patient was treated with intravenous fluids and stress‐dose steroids, and electrolyte abnormalities were corrected. Biopsies from the EGD and colonoscopy demonstrated numerous larvae within the mucosa of the body and antrum of the stomach, as well as duodenum. There were also rare detached larvae seen in the esophagus, and a few larvae within the ileal mucosa.

The patient appears to have Strongyloides hyperinfection, something he is at clear risk for, given his country of origin and his high‐dose corticosteroids. In retrospect, I was dissuaded from seriously considering a diagnosis of parasitic infection in large part because of the absence of peripheral eosinophilia, but this may not be seen in cases of hyperinfection. Additional clues, again in retrospect, were the repeated abscesses with bowel flora and the seemingly nonspecific abdominal rash. I would treat with a course of ivermectin, and carefully monitor his response.

The characteristics of the larvae were suggestive of Strongyloides species (Figure 3). A subsequent stool test for ova and parasites was positive for Strongyloides larvae. The patient was given a single dose of ivermectin. An endocrinology consultant felt that he did not have adrenal insufficiency, and it was recommended that his steroids be tapered off. He was discharged home once he clinically improved.

Figure 3

Although one or two doses of ivermectin typically suffices for uncomplicated strongyloidiasis, the risk of failure in hyperinfection mandates a longer treatment course. I don't believe this patient has been adequately treated, although the removal of his steroids will be helpful.

He was readmitted 3 days later with recrudescent symptoms, and his stool remained positive for Strongyloides. He received 2 weeks of ivermectin and albendazole, and was ultimately discharged to a rehabilitation facility after a complicated hospital stay. Nine months later, the patient was reported to be doing well.

COMMENTARY

This patient's immigration status from the developing world, high‐dose corticosteroid use, and complex clinical course all suggested the possibility of an underlying chronic infectious process. Although the discussant recognized this early on and later briefly mentioned strongyloidiasis as a potential cause of intestinal obstruction, the diagnosis of Strongyloides hyperinfection was not suspected until incontrovertible evidence for it was obtained on EGD. Failure to make the diagnosis earlier by both the involved clinicians and the discussant probably stemmed largely from two factors: the absence of eosinophilia; and lack of recognition that purpura may be seen in cases of hyperinfection, presumably reflecting larval infiltration of the dermis.1 Although eosinophilia accompanies most cases of stronglyloidiasis and may be very pronounced, patients with hyperinfection syndrome frequently fail to mount an eosinophilic response due to underlying immunosuppression, with eosinophilia absent in 70% of such patients in a study from Taiwan.2

Strongyloides stercoralis is an intestinal nematode that causes strongyloidiasis. It affects as many as 100 million people globally,3 mainly in tropical and subtropical areas, but is also endemic in the Southeastern United States, Europe, and Japan. Risk factors include male sex, White race, alcoholism, working in contact with soil (farmers, coal mine workers, etc.), chronic care institutionalization, and low socioeconomic status. In nonendemic regions, it more commonly affects travelers, immigrants, or military personnel.4, 5

The life cycle of S. stercoralis is complex. Infective larvae penetrate the skin through contact with contaminated soil, enter the venous system via lymphatics, and travel to the lung.4, 6 Here, they ascend the tracheobronchial tree and migrate to the gut. In the intestine, larvae develop into adult female worms that burrow into the intestinal mucosa. These worms lay eggs that develop into noninfective rhabditiform larvae, which are then expelled in the stool. Some of the rhabditiform larvae, however, develop into infective filariform larvae, which may penetrate colonic mucosa or perianal skin, enter the bloodstream, and lead to the cycle of autoinfection and chronic strongyloidiasis (carrier state). Autoinfection typically involves a low parasite burden, and is controlled by both host immune factors as well as parasitic factors.7 The mechanism of autoinfection can lead to the persistence of strongyloidiasis for decades after the initial infection, as has been documented in former World War II prisoners of war.8

Factors leading to the impairment of cell‐mediated immunity predispose chronically infected individuals to hyperinfection, as occurred in this patient. The most important of these are corticosteroid administration and Human T‐lymphotropic virus Type‐1 (HTLV‐1) infection, both of which cause significant derangement in TH1/TH2 immune system balance.5, 9 In the hyperinfection syndrome, the burden of parasites increases dramatically, leading to a variety of clinical manifestations. Gastrointestinal phenomena frequently predominate, including watery diarrhea, anorexia, weight loss, nausea/vomiting, gastrointestinal bleeding, and occasionally small bowel obstruction. Pulmonary manifestations are likewise common, and include cough, dyspnea, and wheezing. Cutaneous findings are not uncommon, classically pruritic linear lesions of the abdomen, buttocks, and lower extremities which may be rapidly migratory (larva currens), although purpura and petechiae as displayed by our patient appear to be under‐recognized findings in hyperinfection.2, 5 Gram‐negative bacillary meningitis has been well reported as a complication of migrating larvae, and a wide variety of other organs may rarely be involved.5, 10

The presence of chronic strongyloidiasis should be suspected in patients with ongoing gastrointestinal and/or pulmonary symptoms, or unexplained eosinophilia with a potential exposure history, such as immigrants from Southeast Asia. Diagnosis in these individuals is currently most often made serologically, although stool exam provides a somewhat higher specificity for active infection, at the expense of lower sensitivity.3, 11 In the setting of hyperinfection, stool studies are almost uniformly positive for S. stercoralis, and sputum may be diagnostic as well. Consequently, failure to reach the diagnosis usually reflects a lack of clinical suspicion.5

The therapy of choice for strongyloidiasis is currently ivermectin, with a single dose repeated once, 2 weeks later, highly efficacious in eradicating chronic infection. Treatment of hyperinfection is more challenging and less well studied, but clearly necessitates a more prolonged course of treatment. Many experts advocate treating until worms are no longer present in the stool; some have suggested the combination of ivermectin and albendazole as this patient received, although this has not been examined in controlled fashion.

The diagnosis of Strongyloides hyperinfection is typically delayed or missed because of the failure to consider it, with reported mortality rates as high as 50% in hyperinfection and 87% in disseminated disease.3, 12, 13 This patient fortunately was diagnosed, albeit in delayed fashion, proving the maxim better late than never. His case highlights the need for increased clinical awareness of strongyloidiasis, and specifically the need to consider the possibility of chronic Strongyloides infection prior to administering immunosuppressive medications. In particular, serologic screening of individuals from highly endemic areas for strongyloidiasis, when initiating extended courses of corticosteroids, seems prudent.13

A 59‐year‐old man presented to the emergency department with the acute onset of right‐sided abdominal and flank pain. The pain had begun the previous night, was constant and progressively worsening, and radiated to his right groin. He denied fever, nausea, emesis, or change in his bowel habits, but he did notice mild right lower quadrant discomfort with micturition. Upon further questioning, he also complained of mild dyspnea on climbing stairs and an unspecified recent weight loss.

The most common cause of acute severe right‐sided flank and abdominal pain radiating to the groin and associated with dysuria in a middle‐aged man is ureteral colic. Other etiologies important to consider include retrocecal appendicitis, pyelonephritis, and, rarely, a dissecting abdominal aortic aneurysm. This patient's seemingly recent onset exertional dyspnea and weight loss do not neatly fit any of the above, however.

His past medical history was significant for diabetes mellitus and pemphigus vulgaris diagnosed 7 months previously. He had been treated with prednisone, and the dose decreased from 100 to 60 mg daily, 1 month previously, due to poor glycemic control as well as steroid‐induced neuropathy and myopathy. His other medications included naproxen sodium and ibuprofen for back pain, azathioprine, insulin, pioglitazone, and glimiperide. He had no past surgical history. He had lived in the United States since his emigration from Thailand in 1971. His last trip to Thailand was 5 years previously. He was a taxi cab driver. He had a ten‐pack year history of tobacco use, but had quit 20 years prior. He denied history of alcohol or intravenous drug use.

Pemphigus vulgaris is unlikely to be directly related to this patient's presentation, but in light of his poorly controlled diabetes, his azathioprine use, and particularly his high‐dose corticosteroids, he is certainly immunocompromised. Accordingly, a disseminated infection, either newly acquired or reactivated, merits consideration. His history of residence in, and subsequent travel to, Southeast Asia raises the possibility of several diseases, each of which may be protean in their manifestations; these include tuberculosis, melioidosis, and penicilliosis (infection with Penicillium marneffei). The first two may reactivate long after initial exposure, particularly with insults to the immune system. The same is probably true of penicilliosis, although I am not certain of this. On a slightly less exotic note, domestically acquired infection with histoplasmosis or other endemic fungi is possible.

On examination he was afebrile, had a pulse of 130 beats per minute and a blood pressure of 65/46 mmHg. His oxygen saturation was 92%. He appeared markedly cushingoid, and had mild pallor and generalized weakness. Cardiopulmonary examination was unremarkable. His abdominal exam was notable for distention and hypoactive bowel sounds, with tenderness and firmness to palpation on the right side. Peripheral pulses were normal. Examination of the skin demonstrated ecchymoses over the bilateral forearms, and several healed pemphigus lesions on the abdomen and upper extremities.

The patient's severely deranged hemodynamic parameters indicate either current or impending shock, and resuscitative measures should proceed in tandem with diagnostic efforts. The cause of his shock seems most likely to be either hypovolemic (abdominal wall or intra‐abdominal hemorrhage, or conceivably massive third spacing from an intra‐abdominal catastrophe), or distributive (sepsis, or acute adrenal insufficiency if he has missed recent steroid doses). His ecchymoses may simply reflect chronic glucocorticoid use, but also raise suspicion for a coagulopathy. Provided the patient can be stabilized to allow this, I would urgently obtain a computed tomography (CT) scan of the abdomen and pelvis.

Initial laboratory studies demonstrated a hemoglobin of 9.1 g/dL, white blood cell count 8000/L with 33% bands, 48% segmented neutrophils, 18% lymphocytes, and 0.7% eosinophils, platelet count 356,000/L, sodium 128 mmol/L, BUN 52 mg/dL, creatinine 2.3 mg/dL, and glucose of 232 mg/dL. Coagulation studies were normal, and lactic acid was 1.8 mmol/L (normal range, 0.7‐2.1). Fibrinogen was normal at 591 and LDH was mildly elevated at 654 (normal range, 313‐618 U/L). Total protein and albumin were 3.6 and 1.9 g/dL, respectively. Total bilirubin was 0.6 mg/dL. Random serum cortisol was 20.2 g/dL. Liver enzymes, amylase, lipase, iron stores, B₁₂, folate, and stool for occult blood were normal. Initial cardiac biomarkers were negative, but subsequent troponin‐I was 3.81 ng/mL (elevated, >1.00). Urinalysis showed 0‐4 white blood cells per high powered field.

The laboratory studies provide a variety of useful, albeit nonspecific, information. The high percentage of band forms on white blood cell differential further raises concern for an infectious process, although severe noninfectious stress can also cause this. While we do not know whether the patient's renal failure is acute, I suspect that it is, and may result from a variety of insults including sepsis, hypotension, and volume depletion. His moderately elevated troponin‐I likely reflects supplydemand mismatch or sepsis. I would like to see an electrocardiogram, and I remain very interested in obtaining abdominal imaging.

Chest radiography showed pulmonary vascular congestion without evidence of pneumothorax. Computed tomography scan of the abdomen and pelvis showed retroperitoneal fluid bilaterally (Figure 1). This was described as suspicious for ascites versus hemorrhage, but no obvious source of bleeding was identified. There was also a small amount of right perinephric fluid, but no evidence of a renal mass. The abdominal aorta was normal; there was no lymphadenopathy.

Figure 1

The CT image appears to speak against simple ascites, and seems most consistent with either blood or an infectious process. Consequently, the loculated right retroperitoneal collection should be aspirated, and fluid sent for fungal, acid‐fast, and modified acid‐fast (i.e., for Nocardia) stains and culture, in addition to Gram stain and routine aerobic and anaerobic cultures.

The patient was admitted to the intensive care unit. Stress‐dose steroids were administered, and he improved after resuscitation with fluid and blood. His renal function normalized. Urine and blood cultures returned negative. His hematocrit and multiple repeat CT scans of the abdomen remained stable. A retroperitoneal hemorrhage was diagnosed, and surgical intervention was deemed unnecessary. Both adenosine thallium stress test and echocardiogram were normal. He was continued on 60 mg prednisone daily and discharged home with outpatient follow‐up.

This degree of improvement with volume expansion (and steroids) suggests the patient was markedly volume depleted upon presentation. Although a formal adrenocorticotropic hormone (ACTH) stimulation test was apparently not performed, the random cortisol level suggests adrenal insufficiency was unlikely to have been primarily responsible. While retroperitoneal hemorrhage is possible, the loculated appearance of the collection suggests infection is more likely.

Three weeks later, he was readmitted with recurrent right‐sided abdominal and flank pain. His temperature was 101.3F, and he was tachycardic and hypotensive. His examination was similar to that at the time of his previous presentation. Laboratory data revealed white blood cell count of 13,100/L with 43% bands, hemoglobin of 9.2 g/dL, glucose of 343 mg/dL, bicarbonate 25 mmol/L, normal anion gap and renal function, and lactic acid of 4.5 mmol/L. Liver function tests were normal except for an albumin of 3.0 g/dL. CT scan of the abdomen revealed loculated retroperitoneal fluid collections, increased in size since the prior scan.

The patient is once again evidencing at least early shock, manifested in his deranged hemodynamics and elevated lactate level. I remain puzzled by the fact that he appeared to respond to fluids alone at the time of his initial hospital stay, unless adrenal insufficiency played a greater role than I suspected. Of note, acute adrenal insufficiency could explain much of the current picture, including fever, and bland (uninfected) hematomas are an underappreciated cause of both fever and leukocytosis. Having said this, I remain concerned that his retroperitoneal fluid collections represent abscesses. The most accessible of these should be sampled.

Aspiration of the retroperitoneal fluid yielded purulent material which grew Klebsiella pneumoniae. The cultures were negative for mycobacteria and fungus. Blood and urine cultures were negative. Drains were placed, and he was followed as an outpatient. His fever and leukocytosis subsided, and he completed a 6‐week course of trimethoprim‐sulfamethoxazole. CT imaging confirmed complete evacuation of the fluid.

Retroperitoneal abscesses frequently present in smoldering fashion, although patients may be quite ill by the time of presentation. Most of these are secondary, i.e., they arise from another abnormality in the retroperitoneum. Most commonly this is in the large bowel, kidney, pancreas, or spine. I would carefully scour his follow‐up imaging for additional clues and, if unrevealing, proceed to colonoscopy.

He returned 1 month after drain removal, with 2‐3 days of nausea and abdominal pain. His abdomen was moderately distended but nontender, and multiple persistent petechial and purpuric lesions were present on the upper back, chest, torso, and arms. Abdominal CT scan revealed small bowel obstruction and a collection of fluid in the left paracolic gutter extending into the left retrorenal space.

The patient does not appear to have obvious risk factors for developing a small bowel obstruction. No mention is made of the presence or absence of a transition point on the CT scan, and this should be ascertained. His left‐sided abdominal fluid collection is probably infectious in nature, and I continue to be suspicious of a large bowel (or distal small bowel) source, via either gut perforation or bacterial translocation. The collection needs to be percutaneously drained for both diagnostic and therapeutic reasons, and broadly cultured. Finally, we need to account for the described dermatologic manifestations. The purpuric/petechial lesions sound vasculitic rather than thrombocytopenic in origin based on location; conversely, they may simply reflect a corticosteroid‐related adverse effect. I would like to know whether the purpura was palpable, and to repeat a complete blood count with peripheral smear.

Laboratory data showed hemoglobin of 9.3 g/dL, a platelet count of 444,000/L, and normal coagulation studies. The purpura was nonpalpable (Figure 2). The patient had a nasogastric tube placed for decompression, with bilious drainage. His left retroperitoneal fluid was drained, with cultures yielding Enterococcus faecalis and Enterobacter cloacae. The patient was treated with a course of broad‐spectrum antibiotics. His obstruction improved and the retroperitoneal collection resolved on follow‐up imaging. However, 2 days later, he had recurrent pain; abdominal CT showed a recurrence of small bowel obstruction with an unequivocal transition point in the distal jejunum. A small fluid collection was noted in the left retroperitoneum with a trace of gas in it. He improved with nasogastric suction, his prednisone was tapered to 30 mg daily, and he was discharged home.

Figure 2

The isolation of both Enterococcus and Enterobacter species from his fluid collection, along with the previous isolation of Klebsiella, strongly suggest a bowel source for his recurrent abscesses. Based on this CT report, the patient has clear evidence of at least partial small bowel obstruction. He lacks a history of prior abdominal surgery or other more typical reasons for obstruction caused by extrinsic compression, such as hernia, although it is possible his recurrent abdominal infections may have led to obstruction due to scarring and adhesions. An intraluminal cause of obstruction also needs to be considered, with causes including malignancy (lymphoma, carcinoid, and adenocarcinoma), Crohn's disease, and infections including tuberculosis as well as parasites such as Taenia and Strongyloides. While the purpura is concerning, given the nonpalpable character along with a normal platelet count and coagulation studies, it may be reasonable to provisionally attribute it to high‐dose corticosteroid use.

He was admitted a fourth time a week after being discharged, with nausea, generalized weakness, and weight loss. At presentation, he had a blood pressure of 95/65 mmHg. His white blood cell count was 5,900/L, with 79% neutrophils and 20% bands. An AM cortisol was 18.8 /dL. He was thought to have adrenal insufficiency from steroid withdrawal, was treated with intravenous fluids and steroids, and discharged on a higher dose of prednisone at 60 mg daily. One week later, he again returned to the hospital with watery diarrhea, emesis, and generalized weakness. His blood pressure was 82/50 mmHg, and his abdomen appeared benign. He also had an erythematous rash over his mid‐abdomen. Laboratory data was significant for a sodium of 127 mmol/L, potassium of 3.0 mmol/L, chloride of 98 mmol/L, bicarbonate of 26 mmol/L, glucose of 40 mg/dL, lactate of 14 mmol/L, and albumin of 1.0 g/dL. Stool assay for Clostridium difficile was negative. A CT scan of the abdomen and pelvis showed small bilateral pleural effusions and small bowel fluid consistent with gastroenteritis, but without signs of obstruction. Esophagogastroduodenoscopy (EGD) showed bile backwash into the stomach, as well as inflammatory changes in the proximal and mid‐stomach, and inflammatory reaction and edema in the proximal duodenum. Colonoscopy showed normal appearing ileum and colon.

The patient's latest laboratory values appear to reflect his chronic illness and superimposed diarrhea. I am perplexed by his markedly elevated serum lactate value in association with a normal bicarbonate and low anion gap, and would repeat the lactate level to ensure this is not spurious. His hypoglycemia probably reflects a failure to adjust or discontinue his diabetic medications, although both hypoglycemia and type B lactic acidosis are occasionally manifestations of a paraneoplastic syndrome. The normal colonoscopy findings are helpful in exonerating the colon, provided the preparation was adequate. Presumably, the abnormal areas of the stomach and duodenum were biopsied; I remain suspicious that the answer may lie in the jejunum.

The patient was treated with intravenous fluids and stress‐dose steroids, and electrolyte abnormalities were corrected. Biopsies from the EGD and colonoscopy demonstrated numerous larvae within the mucosa of the body and antrum of the stomach, as well as duodenum. There were also rare detached larvae seen in the esophagus, and a few larvae within the ileal mucosa.

The patient appears to have Strongyloides hyperinfection, something he is at clear risk for, given his country of origin and his high‐dose corticosteroids. In retrospect, I was dissuaded from seriously considering a diagnosis of parasitic infection in large part because of the absence of peripheral eosinophilia, but this may not be seen in cases of hyperinfection. Additional clues, again in retrospect, were the repeated abscesses with bowel flora and the seemingly nonspecific abdominal rash. I would treat with a course of ivermectin, and carefully monitor his response.

The characteristics of the larvae were suggestive of Strongyloides species (Figure 3). A subsequent stool test for ova and parasites was positive for Strongyloides larvae. The patient was given a single dose of ivermectin. An endocrinology consultant felt that he did not have adrenal insufficiency, and it was recommended that his steroids be tapered off. He was discharged home once he clinically improved.

Figure 3

Although one or two doses of ivermectin typically suffices for uncomplicated strongyloidiasis, the risk of failure in hyperinfection mandates a longer treatment course. I don't believe this patient has been adequately treated, although the removal of his steroids will be helpful.

He was readmitted 3 days later with recrudescent symptoms, and his stool remained positive for Strongyloides. He received 2 weeks of ivermectin and albendazole, and was ultimately discharged to a rehabilitation facility after a complicated hospital stay. Nine months later, the patient was reported to be doing well.

COMMENTARY

This patient's immigration status from the developing world, high‐dose corticosteroid use, and complex clinical course all suggested the possibility of an underlying chronic infectious process. Although the discussant recognized this early on and later briefly mentioned strongyloidiasis as a potential cause of intestinal obstruction, the diagnosis of Strongyloides hyperinfection was not suspected until incontrovertible evidence for it was obtained on EGD. Failure to make the diagnosis earlier by both the involved clinicians and the discussant probably stemmed largely from two factors: the absence of eosinophilia; and lack of recognition that purpura may be seen in cases of hyperinfection, presumably reflecting larval infiltration of the dermis.1 Although eosinophilia accompanies most cases of stronglyloidiasis and may be very pronounced, patients with hyperinfection syndrome frequently fail to mount an eosinophilic response due to underlying immunosuppression, with eosinophilia absent in 70% of such patients in a study from Taiwan.2

Strongyloides stercoralis is an intestinal nematode that causes strongyloidiasis. It affects as many as 100 million people globally,3 mainly in tropical and subtropical areas, but is also endemic in the Southeastern United States, Europe, and Japan. Risk factors include male sex, White race, alcoholism, working in contact with soil (farmers, coal mine workers, etc.), chronic care institutionalization, and low socioeconomic status. In nonendemic regions, it more commonly affects travelers, immigrants, or military personnel.4, 5

The life cycle of S. stercoralis is complex. Infective larvae penetrate the skin through contact with contaminated soil, enter the venous system via lymphatics, and travel to the lung.4, 6 Here, they ascend the tracheobronchial tree and migrate to the gut. In the intestine, larvae develop into adult female worms that burrow into the intestinal mucosa. These worms lay eggs that develop into noninfective rhabditiform larvae, which are then expelled in the stool. Some of the rhabditiform larvae, however, develop into infective filariform larvae, which may penetrate colonic mucosa or perianal skin, enter the bloodstream, and lead to the cycle of autoinfection and chronic strongyloidiasis (carrier state). Autoinfection typically involves a low parasite burden, and is controlled by both host immune factors as well as parasitic factors.7 The mechanism of autoinfection can lead to the persistence of strongyloidiasis for decades after the initial infection, as has been documented in former World War II prisoners of war.8

Factors leading to the impairment of cell‐mediated immunity predispose chronically infected individuals to hyperinfection, as occurred in this patient. The most important of these are corticosteroid administration and Human T‐lymphotropic virus Type‐1 (HTLV‐1) infection, both of which cause significant derangement in TH1/TH2 immune system balance.5, 9 In the hyperinfection syndrome, the burden of parasites increases dramatically, leading to a variety of clinical manifestations. Gastrointestinal phenomena frequently predominate, including watery diarrhea, anorexia, weight loss, nausea/vomiting, gastrointestinal bleeding, and occasionally small bowel obstruction. Pulmonary manifestations are likewise common, and include cough, dyspnea, and wheezing. Cutaneous findings are not uncommon, classically pruritic linear lesions of the abdomen, buttocks, and lower extremities which may be rapidly migratory (larva currens), although purpura and petechiae as displayed by our patient appear to be under‐recognized findings in hyperinfection.2, 5 Gram‐negative bacillary meningitis has been well reported as a complication of migrating larvae, and a wide variety of other organs may rarely be involved.5, 10

The presence of chronic strongyloidiasis should be suspected in patients with ongoing gastrointestinal and/or pulmonary symptoms, or unexplained eosinophilia with a potential exposure history, such as immigrants from Southeast Asia. Diagnosis in these individuals is currently most often made serologically, although stool exam provides a somewhat higher specificity for active infection, at the expense of lower sensitivity.3, 11 In the setting of hyperinfection, stool studies are almost uniformly positive for S. stercoralis, and sputum may be diagnostic as well. Consequently, failure to reach the diagnosis usually reflects a lack of clinical suspicion.5

The therapy of choice for strongyloidiasis is currently ivermectin, with a single dose repeated once, 2 weeks later, highly efficacious in eradicating chronic infection. Treatment of hyperinfection is more challenging and less well studied, but clearly necessitates a more prolonged course of treatment. Many experts advocate treating until worms are no longer present in the stool; some have suggested the combination of ivermectin and albendazole as this patient received, although this has not been examined in controlled fashion.

The diagnosis of Strongyloides hyperinfection is typically delayed or missed because of the failure to consider it, with reported mortality rates as high as 50% in hyperinfection and 87% in disseminated disease.3, 12, 13 This patient fortunately was diagnosed, albeit in delayed fashion, proving the maxim better late than never. His case highlights the need for increased clinical awareness of strongyloidiasis, and specifically the need to consider the possibility of chronic Strongyloides infection prior to administering immunosuppressive medications. In particular, serologic screening of individuals from highly endemic areas for strongyloidiasis, when initiating extended courses of corticosteroids, seems prudent.13

A 59‐year‐old man presented to the emergency department with the acute onset of right‐sided abdominal and flank pain. The pain had begun the previous night, was constant and progressively worsening, and radiated to his right groin. He denied fever, nausea, emesis, or change in his bowel habits, but he did notice mild right lower quadrant discomfort with micturition. Upon further questioning, he also complained of mild dyspnea on climbing stairs and an unspecified recent weight loss.

The most common cause of acute severe right‐sided flank and abdominal pain radiating to the groin and associated with dysuria in a middle‐aged man is ureteral colic. Other etiologies important to consider include retrocecal appendicitis, pyelonephritis, and, rarely, a dissecting abdominal aortic aneurysm. This patient's seemingly recent onset exertional dyspnea and weight loss do not neatly fit any of the above, however.

His past medical history was significant for diabetes mellitus and pemphigus vulgaris diagnosed 7 months previously. He had been treated with prednisone, and the dose decreased from 100 to 60 mg daily, 1 month previously, due to poor glycemic control as well as steroid‐induced neuropathy and myopathy. His other medications included naproxen sodium and ibuprofen for back pain, azathioprine, insulin, pioglitazone, and glimiperide. He had no past surgical history. He had lived in the United States since his emigration from Thailand in 1971. His last trip to Thailand was 5 years previously. He was a taxi cab driver. He had a ten‐pack year history of tobacco use, but had quit 20 years prior. He denied history of alcohol or intravenous drug use.

Pemphigus vulgaris is unlikely to be directly related to this patient's presentation, but in light of his poorly controlled diabetes, his azathioprine use, and particularly his high‐dose corticosteroids, he is certainly immunocompromised. Accordingly, a disseminated infection, either newly acquired or reactivated, merits consideration. His history of residence in, and subsequent travel to, Southeast Asia raises the possibility of several diseases, each of which may be protean in their manifestations; these include tuberculosis, melioidosis, and penicilliosis (infection with Penicillium marneffei). The first two may reactivate long after initial exposure, particularly with insults to the immune system. The same is probably true of penicilliosis, although I am not certain of this. On a slightly less exotic note, domestically acquired infection with histoplasmosis or other endemic fungi is possible.

On examination he was afebrile, had a pulse of 130 beats per minute and a blood pressure of 65/46 mmHg. His oxygen saturation was 92%. He appeared markedly cushingoid, and had mild pallor and generalized weakness. Cardiopulmonary examination was unremarkable. His abdominal exam was notable for distention and hypoactive bowel sounds, with tenderness and firmness to palpation on the right side. Peripheral pulses were normal. Examination of the skin demonstrated ecchymoses over the bilateral forearms, and several healed pemphigus lesions on the abdomen and upper extremities.

The patient's severely deranged hemodynamic parameters indicate either current or impending shock, and resuscitative measures should proceed in tandem with diagnostic efforts. The cause of his shock seems most likely to be either hypovolemic (abdominal wall or intra‐abdominal hemorrhage, or conceivably massive third spacing from an intra‐abdominal catastrophe), or distributive (sepsis, or acute adrenal insufficiency if he has missed recent steroid doses). His ecchymoses may simply reflect chronic glucocorticoid use, but also raise suspicion for a coagulopathy. Provided the patient can be stabilized to allow this, I would urgently obtain a computed tomography (CT) scan of the abdomen and pelvis.

Initial laboratory studies demonstrated a hemoglobin of 9.1 g/dL, white blood cell count 8000/L with 33% bands, 48% segmented neutrophils, 18% lymphocytes, and 0.7% eosinophils, platelet count 356,000/L, sodium 128 mmol/L, BUN 52 mg/dL, creatinine 2.3 mg/dL, and glucose of 232 mg/dL. Coagulation studies were normal, and lactic acid was 1.8 mmol/L (normal range, 0.7‐2.1). Fibrinogen was normal at 591 and LDH was mildly elevated at 654 (normal range, 313‐618 U/L). Total protein and albumin were 3.6 and 1.9 g/dL, respectively. Total bilirubin was 0.6 mg/dL. Random serum cortisol was 20.2 g/dL. Liver enzymes, amylase, lipase, iron stores, B₁₂, folate, and stool for occult blood were normal. Initial cardiac biomarkers were negative, but subsequent troponin‐I was 3.81 ng/mL (elevated, >1.00). Urinalysis showed 0‐4 white blood cells per high powered field.

The laboratory studies provide a variety of useful, albeit nonspecific, information. The high percentage of band forms on white blood cell differential further raises concern for an infectious process, although severe noninfectious stress can also cause this. While we do not know whether the patient's renal failure is acute, I suspect that it is, and may result from a variety of insults including sepsis, hypotension, and volume depletion. His moderately elevated troponin‐I likely reflects supplydemand mismatch or sepsis. I would like to see an electrocardiogram, and I remain very interested in obtaining abdominal imaging.

Chest radiography showed pulmonary vascular congestion without evidence of pneumothorax. Computed tomography scan of the abdomen and pelvis showed retroperitoneal fluid bilaterally (Figure 1). This was described as suspicious for ascites versus hemorrhage, but no obvious source of bleeding was identified. There was also a small amount of right perinephric fluid, but no evidence of a renal mass. The abdominal aorta was normal; there was no lymphadenopathy.

Figure 1

The CT image appears to speak against simple ascites, and seems most consistent with either blood or an infectious process. Consequently, the loculated right retroperitoneal collection should be aspirated, and fluid sent for fungal, acid‐fast, and modified acid‐fast (i.e., for Nocardia) stains and culture, in addition to Gram stain and routine aerobic and anaerobic cultures.

The patient was admitted to the intensive care unit. Stress‐dose steroids were administered, and he improved after resuscitation with fluid and blood. His renal function normalized. Urine and blood cultures returned negative. His hematocrit and multiple repeat CT scans of the abdomen remained stable. A retroperitoneal hemorrhage was diagnosed, and surgical intervention was deemed unnecessary. Both adenosine thallium stress test and echocardiogram were normal. He was continued on 60 mg prednisone daily and discharged home with outpatient follow‐up.

This degree of improvement with volume expansion (and steroids) suggests the patient was markedly volume depleted upon presentation. Although a formal adrenocorticotropic hormone (ACTH) stimulation test was apparently not performed, the random cortisol level suggests adrenal insufficiency was unlikely to have been primarily responsible. While retroperitoneal hemorrhage is possible, the loculated appearance of the collection suggests infection is more likely.

Three weeks later, he was readmitted with recurrent right‐sided abdominal and flank pain. His temperature was 101.3F, and he was tachycardic and hypotensive. His examination was similar to that at the time of his previous presentation. Laboratory data revealed white blood cell count of 13,100/L with 43% bands, hemoglobin of 9.2 g/dL, glucose of 343 mg/dL, bicarbonate 25 mmol/L, normal anion gap and renal function, and lactic acid of 4.5 mmol/L. Liver function tests were normal except for an albumin of 3.0 g/dL. CT scan of the abdomen revealed loculated retroperitoneal fluid collections, increased in size since the prior scan.

The patient is once again evidencing at least early shock, manifested in his deranged hemodynamics and elevated lactate level. I remain puzzled by the fact that he appeared to respond to fluids alone at the time of his initial hospital stay, unless adrenal insufficiency played a greater role than I suspected. Of note, acute adrenal insufficiency could explain much of the current picture, including fever, and bland (uninfected) hematomas are an underappreciated cause of both fever and leukocytosis. Having said this, I remain concerned that his retroperitoneal fluid collections represent abscesses. The most accessible of these should be sampled.

Aspiration of the retroperitoneal fluid yielded purulent material which grew Klebsiella pneumoniae. The cultures were negative for mycobacteria and fungus. Blood and urine cultures were negative. Drains were placed, and he was followed as an outpatient. His fever and leukocytosis subsided, and he completed a 6‐week course of trimethoprim‐sulfamethoxazole. CT imaging confirmed complete evacuation of the fluid.

Retroperitoneal abscesses frequently present in smoldering fashion, although patients may be quite ill by the time of presentation. Most of these are secondary, i.e., they arise from another abnormality in the retroperitoneum. Most commonly this is in the large bowel, kidney, pancreas, or spine. I would carefully scour his follow‐up imaging for additional clues and, if unrevealing, proceed to colonoscopy.

He returned 1 month after drain removal, with 2‐3 days of nausea and abdominal pain. His abdomen was moderately distended but nontender, and multiple persistent petechial and purpuric lesions were present on the upper back, chest, torso, and arms. Abdominal CT scan revealed small bowel obstruction and a collection of fluid in the left paracolic gutter extending into the left retrorenal space.

The patient does not appear to have obvious risk factors for developing a small bowel obstruction. No mention is made of the presence or absence of a transition point on the CT scan, and this should be ascertained. His left‐sided abdominal fluid collection is probably infectious in nature, and I continue to be suspicious of a large bowel (or distal small bowel) source, via either gut perforation or bacterial translocation. The collection needs to be percutaneously drained for both diagnostic and therapeutic reasons, and broadly cultured. Finally, we need to account for the described dermatologic manifestations. The purpuric/petechial lesions sound vasculitic rather than thrombocytopenic in origin based on location; conversely, they may simply reflect a corticosteroid‐related adverse effect. I would like to know whether the purpura was palpable, and to repeat a complete blood count with peripheral smear.

Laboratory data showed hemoglobin of 9.3 g/dL, a platelet count of 444,000/L, and normal coagulation studies. The purpura was nonpalpable (Figure 2). The patient had a nasogastric tube placed for decompression, with bilious drainage. His left retroperitoneal fluid was drained, with cultures yielding Enterococcus faecalis and Enterobacter cloacae. The patient was treated with a course of broad‐spectrum antibiotics. His obstruction improved and the retroperitoneal collection resolved on follow‐up imaging. However, 2 days later, he had recurrent pain; abdominal CT showed a recurrence of small bowel obstruction with an unequivocal transition point in the distal jejunum. A small fluid collection was noted in the left retroperitoneum with a trace of gas in it. He improved with nasogastric suction, his prednisone was tapered to 30 mg daily, and he was discharged home.

Figure 2

The isolation of both Enterococcus and Enterobacter species from his fluid collection, along with the previous isolation of Klebsiella, strongly suggest a bowel source for his recurrent abscesses. Based on this CT report, the patient has clear evidence of at least partial small bowel obstruction. He lacks a history of prior abdominal surgery or other more typical reasons for obstruction caused by extrinsic compression, such as hernia, although it is possible his recurrent abdominal infections may have led to obstruction due to scarring and adhesions. An intraluminal cause of obstruction also needs to be considered, with causes including malignancy (lymphoma, carcinoid, and adenocarcinoma), Crohn's disease, and infections including tuberculosis as well as parasites such as Taenia and Strongyloides. While the purpura is concerning, given the nonpalpable character along with a normal platelet count and coagulation studies, it may be reasonable to provisionally attribute it to high‐dose corticosteroid use.

He was admitted a fourth time a week after being discharged, with nausea, generalized weakness, and weight loss. At presentation, he had a blood pressure of 95/65 mmHg. His white blood cell count was 5,900/L, with 79% neutrophils and 20% bands. An AM cortisol was 18.8 /dL. He was thought to have adrenal insufficiency from steroid withdrawal, was treated with intravenous fluids and steroids, and discharged on a higher dose of prednisone at 60 mg daily. One week later, he again returned to the hospital with watery diarrhea, emesis, and generalized weakness. His blood pressure was 82/50 mmHg, and his abdomen appeared benign. He also had an erythematous rash over his mid‐abdomen. Laboratory data was significant for a sodium of 127 mmol/L, potassium of 3.0 mmol/L, chloride of 98 mmol/L, bicarbonate of 26 mmol/L, glucose of 40 mg/dL, lactate of 14 mmol/L, and albumin of 1.0 g/dL. Stool assay for Clostridium difficile was negative. A CT scan of the abdomen and pelvis showed small bilateral pleural effusions and small bowel fluid consistent with gastroenteritis, but without signs of obstruction. Esophagogastroduodenoscopy (EGD) showed bile backwash into the stomach, as well as inflammatory changes in the proximal and mid‐stomach, and inflammatory reaction and edema in the proximal duodenum. Colonoscopy showed normal appearing ileum and colon.

The patient's latest laboratory values appear to reflect his chronic illness and superimposed diarrhea. I am perplexed by his markedly elevated serum lactate value in association with a normal bicarbonate and low anion gap, and would repeat the lactate level to ensure this is not spurious. His hypoglycemia probably reflects a failure to adjust or discontinue his diabetic medications, although both hypoglycemia and type B lactic acidosis are occasionally manifestations of a paraneoplastic syndrome. The normal colonoscopy findings are helpful in exonerating the colon, provided the preparation was adequate. Presumably, the abnormal areas of the stomach and duodenum were biopsied; I remain suspicious that the answer may lie in the jejunum.

The patient was treated with intravenous fluids and stress‐dose steroids, and electrolyte abnormalities were corrected. Biopsies from the EGD and colonoscopy demonstrated numerous larvae within the mucosa of the body and antrum of the stomach, as well as duodenum. There were also rare detached larvae seen in the esophagus, and a few larvae within the ileal mucosa.

The patient appears to have Strongyloides hyperinfection, something he is at clear risk for, given his country of origin and his high‐dose corticosteroids. In retrospect, I was dissuaded from seriously considering a diagnosis of parasitic infection in large part because of the absence of peripheral eosinophilia, but this may not be seen in cases of hyperinfection. Additional clues, again in retrospect, were the repeated abscesses with bowel flora and the seemingly nonspecific abdominal rash. I would treat with a course of ivermectin, and carefully monitor his response.

The characteristics of the larvae were suggestive of Strongyloides species (Figure 3). A subsequent stool test for ova and parasites was positive for Strongyloides larvae. The patient was given a single dose of ivermectin. An endocrinology consultant felt that he did not have adrenal insufficiency, and it was recommended that his steroids be tapered off. He was discharged home once he clinically improved.

Figure 3

Although one or two doses of ivermectin typically suffices for uncomplicated strongyloidiasis, the risk of failure in hyperinfection mandates a longer treatment course. I don't believe this patient has been adequately treated, although the removal of his steroids will be helpful.

He was readmitted 3 days later with recrudescent symptoms, and his stool remained positive for Strongyloides. He received 2 weeks of ivermectin and albendazole, and was ultimately discharged to a rehabilitation facility after a complicated hospital stay. Nine months later, the patient was reported to be doing well.

COMMENTARY

This patient's immigration status from the developing world, high‐dose corticosteroid use, and complex clinical course all suggested the possibility of an underlying chronic infectious process. Although the discussant recognized this early on and later briefly mentioned strongyloidiasis as a potential cause of intestinal obstruction, the diagnosis of Strongyloides hyperinfection was not suspected until incontrovertible evidence for it was obtained on EGD. Failure to make the diagnosis earlier by both the involved clinicians and the discussant probably stemmed largely from two factors: the absence of eosinophilia; and lack of recognition that purpura may be seen in cases of hyperinfection, presumably reflecting larval infiltration of the dermis.1 Although eosinophilia accompanies most cases of stronglyloidiasis and may be very pronounced, patients with hyperinfection syndrome frequently fail to mount an eosinophilic response due to underlying immunosuppression, with eosinophilia absent in 70% of such patients in a study from Taiwan.2

Strongyloides stercoralis is an intestinal nematode that causes strongyloidiasis. It affects as many as 100 million people globally,3 mainly in tropical and subtropical areas, but is also endemic in the Southeastern United States, Europe, and Japan. Risk factors include male sex, White race, alcoholism, working in contact with soil (farmers, coal mine workers, etc.), chronic care institutionalization, and low socioeconomic status. In nonendemic regions, it more commonly affects travelers, immigrants, or military personnel.4, 5

The life cycle of S. stercoralis is complex. Infective larvae penetrate the skin through contact with contaminated soil, enter the venous system via lymphatics, and travel to the lung.4, 6 Here, they ascend the tracheobronchial tree and migrate to the gut. In the intestine, larvae develop into adult female worms that burrow into the intestinal mucosa. These worms lay eggs that develop into noninfective rhabditiform larvae, which are then expelled in the stool. Some of the rhabditiform larvae, however, develop into infective filariform larvae, which may penetrate colonic mucosa or perianal skin, enter the bloodstream, and lead to the cycle of autoinfection and chronic strongyloidiasis (carrier state). Autoinfection typically involves a low parasite burden, and is controlled by both host immune factors as well as parasitic factors.7 The mechanism of autoinfection can lead to the persistence of strongyloidiasis for decades after the initial infection, as has been documented in former World War II prisoners of war.8

Factors leading to the impairment of cell‐mediated immunity predispose chronically infected individuals to hyperinfection, as occurred in this patient. The most important of these are corticosteroid administration and Human T‐lymphotropic virus Type‐1 (HTLV‐1) infection, both of which cause significant derangement in TH1/TH2 immune system balance.5, 9 In the hyperinfection syndrome, the burden of parasites increases dramatically, leading to a variety of clinical manifestations. Gastrointestinal phenomena frequently predominate, including watery diarrhea, anorexia, weight loss, nausea/vomiting, gastrointestinal bleeding, and occasionally small bowel obstruction. Pulmonary manifestations are likewise common, and include cough, dyspnea, and wheezing. Cutaneous findings are not uncommon, classically pruritic linear lesions of the abdomen, buttocks, and lower extremities which may be rapidly migratory (larva currens), although purpura and petechiae as displayed by our patient appear to be under‐recognized findings in hyperinfection.2, 5 Gram‐negative bacillary meningitis has been well reported as a complication of migrating larvae, and a wide variety of other organs may rarely be involved.5, 10

The presence of chronic strongyloidiasis should be suspected in patients with ongoing gastrointestinal and/or pulmonary symptoms, or unexplained eosinophilia with a potential exposure history, such as immigrants from Southeast Asia. Diagnosis in these individuals is currently most often made serologically, although stool exam provides a somewhat higher specificity for active infection, at the expense of lower sensitivity.3, 11 In the setting of hyperinfection, stool studies are almost uniformly positive for S. stercoralis, and sputum may be diagnostic as well. Consequently, failure to reach the diagnosis usually reflects a lack of clinical suspicion.5

The therapy of choice for strongyloidiasis is currently ivermectin, with a single dose repeated once, 2 weeks later, highly efficacious in eradicating chronic infection. Treatment of hyperinfection is more challenging and less well studied, but clearly necessitates a more prolonged course of treatment. Many experts advocate treating until worms are no longer present in the stool; some have suggested the combination of ivermectin and albendazole as this patient received, although this has not been examined in controlled fashion.

The diagnosis of Strongyloides hyperinfection is typically delayed or missed because of the failure to consider it, with reported mortality rates as high as 50% in hyperinfection and 87% in disseminated disease.3, 12, 13 This patient fortunately was diagnosed, albeit in delayed fashion, proving the maxim better late than never. His case highlights the need for increased clinical awareness of strongyloidiasis, and specifically the need to consider the possibility of chronic Strongyloides infection prior to administering immunosuppressive medications. In particular, serologic screening of individuals from highly endemic areas for strongyloidiasis, when initiating extended courses of corticosteroids, seems prudent.13

The traditional acute care for the elderly (ACE) unit has demonstrated improved functional outcomes without increased costs or changes in length of stay (LOS).15 It is, however, limited in scope to only those patients cared for on a fixed geographical unit. This structural limitation is of increasing relevance in times of high hospital bed occupancy rates, as during such times, many appropriate older patients are admitted elsewhere. In our experience with a traditional ACE unit‐based model, only 52% of our geriatrics practice patients were admitted to an ACE unit bed, while the remainder were admitted to various medical units throughout the hospital. We therefore abandoned our traditional unit‐based ACE service in July 2007 in favor of a mobile ACE (MACE) service, bringing the interdisciplinary, patient‐centered team approach to our hospitalized older adult patients admitted throughout the hospital.

The purpose of this study is to compare the operational and quality outcomes for patients cared for on the MACE service to those cared for on a unit‐based ACE service and matched controls cared for on other general medical services. We hypothesized that the MACE service would be associated with lower lengths of stay, reduced costs, and decreased rehospitalization rates.

METHODS

The MACE team was composed of a geriatrician‐hospitalist, geriatric medicine fellow, social worker, and nurse coordinator. The geriatric medicine attending on the MACE service was in the hospital providing patient care during regular working hours from Monday through Friday, while the weekends were covered by a rotating group of all geriatric medicine faculty. During the first and second years of MACE, there were 7 and 4 attendings, respectively; all fellowship‐trained geriatricians. Three of the 4 geriatric medicine hospitalists during year 2 had been in practice between 1 and 3 years postfellowship and also had training in palliative medicine, although were not board‐certified in the latter. The fourth hospitalist had been in practice for 5 years postfellowship. The interdisciplinary team met daily to discuss the care of all patients and used a transitional care model based on The Care Transitions Program⁶ adapted to our institution, with a focus on reducing the risks of hazards of hospitalization. Care coordination with the outpatient practice, early family meetings, discharge planning, patient and caregiver education, and postdischarge follow‐up phone calls were some of the key hallmarks of the service (Table 1).

We conducted a retrospective cohort study with propensity‐score matching in an urban academic medical center. Study subjects comprised 5 distinct groups. First were community‐dwelling older adults cared for at our outpatient geriatrics ambulatory practice who were discharged from our traditional ACE unit‐based acute care service at the Mount Sinai Hospital from July 1, 2006 through June 30, 2007 (N = 450). Second and third were patients from the same practice discharged from our MACE service during the first 2 years of operation (N = 556 from July 1, 2007 through June 30, 2008, and N = 501 from July 1, 2008 through June 30, 2009). Fourth and fifth were control cohorts of hospitalized older adults discharged from other medical services at the Mount Sinai Hospital during these same 2 years (N = 4863 and N = 4777, respectively). The average daily census on all services was 1012 patients.

Some patients on all 3 services are co‐managed with house staff, who are responsible for writing physician orders. Control cohort patients were cared for by a mix of private attendings (approximately 75%) or hospitalists (25%), and in contradistinction to MACE patients, their typical care did not include daily interdisciplinary team rounds, a nurse coordinator, or geriatrics fellow. Social work and case management were unit‐ as opposed to team‐based. Care on the ACE unit‐based service differed from care for matched control patients by having daily interdisciplinary team rounds, a prepared environment, and nursing‐led protocols for the patients on the ACE unit.

Because the ACE unit‐based service admitted both patients who were and were not cared for in our ambulatory practice, while the MACE service admitted only patients cared for in the ambulatory practice, we deleted from the study sample the patients who did not have a visit to our outpatient practice before the index hospitalization. This allowed us to isolate the effect of the model of care itself as opposed to the effect of simply changing the patient base for admissions. We then merged the files with the hospital's administrative database and electronic billing system to obtain demographic and claims data.

Additional demographic data were obtained through chart review of the MACE patients during year 1. The chart review process was standardized using a data abstraction instrument and by determining inter‐rater reliability of the individual data abstractors (comprised of author B.K. and 4 MACE team members).

Costs were assigned to individual admissions by the hospital's cost reporting system and include a combination of traceable costs (such as imaging, laboratory, and pharmacy) and applied costs (nursing; allocated based on geographic location in the hospital) to arrive at direct and total costs.

We made 3 distinct comparisons of operational and quality outcomes using the above 5 groups, first comparing patients cared for on our traditional ACE unit‐based service to those cared for on the MACE service, and second and third comparing patients on the MACE service to propensity score‐matched controls during the first and second year of operations. Specifically, we hypothesized that the MACE service would be associated with reduced LOS, costs, and readmission rates compared with the ACE unit‐based service and the matched control groups. We used multivariate logistic regression to estimate the association of binary quality outcomes (mortality during the hospital stay, 7‐ and 30‐day readmission rates) with the existence of MACE while adjusting for confounding variables which included patient demographic and clinical characteristics such as age, gender, race, total number of comorbidities (calculated by Elixhauser method that includes 30 categories of comorbid illnesses identified by secondary diagnosis codes and discharge diagnosis‐related groups [DRGs]).7 We considered the clustering effect due to the same attending physician into the model as well. While adjusting for the same covariates, we used generalized linear models with a gamma distribution and log link to estimate the association of continuous variables (costs and LOS) with the existence of MACE.

The same statistical methods were applied to the second and third comparisons between patients cared for on the MACE and the propensity score‐matched cohorts for the first and second year of the MACE service. First, 2 control cohorts (N = 6148 and 5803 of our hospital discharges from July 1, 2007 to June 30, 2008, and July 1, 2008 to June 30, 2009, respectively, with age > 64 and with the identical DRG and All Patient Refined DRG (APR DRG) Severity of Illness (SOI) score as those of the MACE groups were obtained from our hospital's administrative database to reduce the selection bias. Then, 4863 patients within the first cohort (N = 6148) and 4777 patients within the second cohort (N = 5,803) with the closest propensity score were matched to 545 of 556 MACE patients and 494 of 501 MACE patients, respectively, in which the logit of their propensity score was within 0.02 standard deviations of the logit of the MACE patient's score.

Propensity scores were determined by logistic regression on whether patients were admitted to the MACE. The covariates for the propensity model were the same as the previously stated adjusting variables. Usual care patients' data were weighted to account for the one‐to‐many propensity score‐matching algorithm.

We similarly conducted a post hoc analysis of MACE compared with a subgroup control cohort of patients cared for by medicine hospitalists in year 1 (N = 1175) and year 2 (N = 1564), with age > 64 and with the identical DRG and APR DRG SOI as those of the MACE group. We then matched 1012 of the 1175 discharges with the closest propensity score to 389 of the 411 MACE discharges who were cared for by 1 of the 4 geriatric medicine hospitalists in year 1 and 1308 of the 1564 discharges to 471 of the 501 MACE discharges in year 2, in which the logit of their propensity score was within 0.02 standard deviations of the logit of the MACE patient's score, using the same covariates described above.

All analyses were done using Stata software, version 9.2 (StataCorp LP, College Station, TX). This project was exempted by the Institutional Review Board at Mount Sinai School of Medicine, New York, New York.

RESULTS

Table 2 presents the characteristics of the study subjects in all 5 groups. Patients cared for on the ACE unit‐based service and the MACE service in years 1 and 2 were very similar, with a mean age of 82.6, 83.2, and 83.6 years; 74.4%, 75.9%, and 76.7% were female; and mean Elixhauser comorbidity scores were 3.4, 3.3, and 3.5, respectively. Patients in the 2 matched control groups were likewise very similar to those in the matched MACE groups with regard to all demographic variables.

Chart review of the year 1 MACE discharges revealed that 70% spoke English as their primary language and 46% had cognitive impairment. Most lived at home alone (49%) or with family members (41%) while receiving some paid caregiver help (59%). The remaining 10% were admitted from either an assisted living facility (5%) or subacute rehabilitation (5%). Only 12% were wheelchair or bed‐bound, while 21% ambulated without and 67% with an assistive device. Their functional status was limited, with 58% dependent for both ADLs and IADLs, 22% dependent for IADLs only, and 20% independent in both. They had relatively high prescription medication burdens, with 10% taking 05, 34% taking 610, 38% taking 1115, and 18% taking >15 medications.

Patients cared for by the MACE service had an adjusted 2.1 days shorter LOS (P 0.001) when compared with patients cared for on the ACE unit service. Additionally, there was a net savings of $2872 in total costs per hospitalization (P = 0.002), $1094 in direct costs (P = 0.016), $849 in nursing costs (P 0.001), and $237 in pharmacy costs (P = 0.002). Imaging and laboratory costs between the 2 groups were not statistically different. There was no significant differences in in‐hospital mortality, 7‐day, 30‐day, or 90‐day readmission rates between the 2 groups (Table 3).

There was no difference in LOS between the MACE patients during the first year of service compared with propensity score‐matched control patients (5.8 vs 6.5 days). There was, however, a net savings of $2453 in total costs per hospitalization (P 0.001), $842 (P = 0.03) in direct costs, $393 in nursing costs (P = 0.026), and $39 in laboratory costs (P = 0.029). Imaging and pharmacy costs between the 2 groups were not statistically different. There was no significant differences in in‐hospital mortality, 7‐day or 30‐day readmission rates between the 2 groups. However, the 90‐day readmission rate was higher in MACE patients (Table 3).

During the second year of the MACE service, however, there was a significant reduction in LOS of 1.6 days (P 0.001), a net savings of $4943 in total costs per hospitalization (P 0.001), $2081 (P 0.001) in direct costs, $937 in nursing costs (P 0.001), $68 in laboratory costs (P 0.001), and $223 in pharmacy costs (P = 0.03). There were no significant differences in imaging costs, in‐hospital mortality, and 7‐day, 30‐day, or 90‐day readmission rates between the 2 groups (Table 3).

A subgroup analysis of the first and second year comparisons including only those patients in the control groups cared for by medicine hospitalists demonstrated reductions in the MACE in total cost in year 1 and LOS, mortality, total, and nursing costs in year 2. However, in year 1, the 30‐day and 90‐day readmission rates were increased in the MACE compared with the control group (Table 4).

We found no differences in a separate post hoc subgroup analysis assessing whether a 3‐month nurse coordinator's leave of absence during year 1 affected year 1 results. The service size was unaffected by her absence, and all patients continued to receive daily visits by the attending and fellow. During this time, other team members took over many of the nurse coordinator roles, except for the postdischarge phone calls.

DISCUSSION

Older adults constitute a disproportionate share of hospital admissions and hospital days. They typically have multiple comorbid conditions, higher rates of cognitive impairment and functional dependence, and complex social situations that all increase their risk of adverse outcomes. Current efforts for national healthcare reform focus on the combined economic and quality imperatives to improve the care of hospitalized older adults. Given the increasing representation of this fastest growing segment of the population in the acute care setting, the geographical unit‐based model for care delivery is untenable in many circumstances. Therefore, we developed a mobile ACE service in an effort to provide the geriatric‐focused acute care found on ACE units to older adults admitted to any medical unit in the hospital.

Our study compared operational and quality outcomes for older patients cared for by our mobile ACE service to those cared for on the unit‐based ACE service and other general medical services. We found a significant reduction in both LOS and costs in all 3 comparisons, except for LOS during the first year of the mobile ACE service. This heightened efficiency was not associated with changes in the quality measures of in‐hospital mortality and 7‐ and 30‐day readmission rates, though the 90‐day readmission rate was slightly higher for the MACE in year 1.

The adjusted total cost savings per admission in years 1 and 2 of approximately $2400 ($12,764 vs $10,311) and $4900 ($15,636 vs $10,693), respectively, translate into an overall annual savings of roughly $1,200,000 (500 patients $2400/patient) in year 1 and $2,450,000 (500 patients $4,900/patient) in year 2. The only relevant cost of the MACE service model compared with the comparison groups is the nurse coordinator salary and benefits, which are paid for by the hospital (as job responsibilities include participation in nursing department quality improvement projects and nursing education) and would not meaningfully offset these savings. The team social worker is a re‐allocation of existing hospital resources, whose salary line is likewise paid for by the hospital.

Our study has several important limitations. First, we lack data on readmissions to other hospitals. Our readmission rates are high compared with the national 19.6% 30‐day Medicare readmission rate cited in a recent study, and we failed to show significant reductions in in‐hospital mortality or 7‐ or 30‐day readmission rates.10 This lack of benefit may be related to control group patients, some of whom receive their community care outside of our institution, being more likely to be readmitted to other hospitals compared with our MACE patients, who were all receiving their ambulatory care in our associated faculty practice. In addition, the high readmission rate on the MACE service may be driven by a relatively small number of patients who are frequently admitted. For example, of the 363 unique MACE patients from year 2, 22 had 3 and 11 had 4 or 5 admissions. We are currently evaluating these 33 patients who accounted for 22% of the admissions to better understand the causes.

A second limitation of the study is selection bias. While patients were very well‐matched through propensity scoring and had identical DRG and DRG‐SOI levels (the latter having been demonstrated in a previous study's regression analysis to be the leading correlate of LOS and cost),9 there may be unaccounted for differences between the patients cared for on the MACE and in the control group. A third limitation is the external validity of our study, which took place in a single large academic medical center in New York City. While the MACE model may very well be readily adaptable elsewhere, numerous studies have demonstrated wide variation in medical practice patterns and healthcare use which may influence the exportability of the model.11, 12 However, our LOS of 5.8 and 5.6 days in years 1 and 2 of the MACE service, respectively, are similar to national data of 5.6 days for hospitalized adults >74 years of age.13

Benefits in cost and LOS reductions may be, in part, due to the hospitalist nature of the model as hospital medicine literature has demonstrated similar reductions for Medicare patients of approximately $1000 and 0.5 days per admission.8, 9 Our findings support this hypothesis as the LOS reduction was not present during the first year of our MACE service during which the hospitalist model was not fully implemented. During this transition phase from the unit‐based ACE to the mobile ACE service, there were 4 physicians who covered more than 75% of on‐service time (10 of the 13 annual 4‐week rotations), while the remaining 25% was covered by 3 physicians (each working 1 block). The following year (July 2008 to June 2009), during which an LOS reduction was demonstrated, a full geriatric medicine hospitalist model was in effect, with patients on the MACE service cared for 100% of the time (excluding weekends) by 1 of 4 geriatric medicine hospitalists. By comparison, 22% and 29% of control group patients were cared for by medicine hospitalists during years 1 and 2, respectively. In addition to this transition to a hospitalist model, there may have been other undefined service improvements over the first year which contributed to the LOS and total cost reductions achieved in year 2 in the hospitalist subgroup analysis. Likewise, the increased 90‐day readmission rates seen in year 1 but not in year 2 in both the main and hospitalist subgroup analyses may be related to MACE service improvements over time. A more vigorous proactive intervention beyond the follow‐up phone call is likely needed to impact 90‐day readmissions.

LOS reductions may also have been related to the interdisciplinary team‐based approach in which a need for family meetings to address goals of care or assess and attempt to resolve complex family/living situations was identified early in the course of hospitalization. Likewise, in New York State, the application process for discharge to a postacute care setting begins with the completion of a Patient Review Instrument (PRI), which contains detailed information on the patient's physical, medical, and cognitive status. The MACE model circumvents the traditional case manager's role of completing the PRI by having the MACE nurse coordinator trained and certified to do so. The daily or twice daily MACE team meeting may have enabled more timely initiation of this early step in the discharge process for these patients, ultimately resulting in a reduced LOS.

An important concern this study is not able to address is whether LOS reductions are achieved at a price of impaired functional status. A prospective longitudinal study on the outcomes of patients cared for by a MACE service that includes detailed assessments of functional status based upon information gathered during admission and postdischarge during follow‐up phone calls is needed to properly evaluate this possibility.

Given the lack of wide‐spread adoption of the traditional ACE unit‐based model of care and its inherent limitations in the setting of high occupancy rates, a mobile ACE service may prove useful in providing high quality clinical care with reduced LOS and costs. This team‐based, as opposed to unit‐based, approach benefits from having low entry costs, as hospital administration can re‐allocate existing resources to fit the model and avoid costly capital investments in specialized unit design and outfitting. Further research should include metrics on functional status, all‐hospital readmission rates, and patient/caregiver satisfaction to better assess the feasibility of this acute care model.

The traditional acute care for the elderly (ACE) unit has demonstrated improved functional outcomes without increased costs or changes in length of stay (LOS).15 It is, however, limited in scope to only those patients cared for on a fixed geographical unit. This structural limitation is of increasing relevance in times of high hospital bed occupancy rates, as during such times, many appropriate older patients are admitted elsewhere. In our experience with a traditional ACE unit‐based model, only 52% of our geriatrics practice patients were admitted to an ACE unit bed, while the remainder were admitted to various medical units throughout the hospital. We therefore abandoned our traditional unit‐based ACE service in July 2007 in favor of a mobile ACE (MACE) service, bringing the interdisciplinary, patient‐centered team approach to our hospitalized older adult patients admitted throughout the hospital.

The purpose of this study is to compare the operational and quality outcomes for patients cared for on the MACE service to those cared for on a unit‐based ACE service and matched controls cared for on other general medical services. We hypothesized that the MACE service would be associated with lower lengths of stay, reduced costs, and decreased rehospitalization rates.

METHODS

The MACE team was composed of a geriatrician‐hospitalist, geriatric medicine fellow, social worker, and nurse coordinator. The geriatric medicine attending on the MACE service was in the hospital providing patient care during regular working hours from Monday through Friday, while the weekends were covered by a rotating group of all geriatric medicine faculty. During the first and second years of MACE, there were 7 and 4 attendings, respectively; all fellowship‐trained geriatricians. Three of the 4 geriatric medicine hospitalists during year 2 had been in practice between 1 and 3 years postfellowship and also had training in palliative medicine, although were not board‐certified in the latter. The fourth hospitalist had been in practice for 5 years postfellowship. The interdisciplinary team met daily to discuss the care of all patients and used a transitional care model based on The Care Transitions Program⁶ adapted to our institution, with a focus on reducing the risks of hazards of hospitalization. Care coordination with the outpatient practice, early family meetings, discharge planning, patient and caregiver education, and postdischarge follow‐up phone calls were some of the key hallmarks of the service (Table 1).

We conducted a retrospective cohort study with propensity‐score matching in an urban academic medical center. Study subjects comprised 5 distinct groups. First were community‐dwelling older adults cared for at our outpatient geriatrics ambulatory practice who were discharged from our traditional ACE unit‐based acute care service at the Mount Sinai Hospital from July 1, 2006 through June 30, 2007 (N = 450). Second and third were patients from the same practice discharged from our MACE service during the first 2 years of operation (N = 556 from July 1, 2007 through June 30, 2008, and N = 501 from July 1, 2008 through June 30, 2009). Fourth and fifth were control cohorts of hospitalized older adults discharged from other medical services at the Mount Sinai Hospital during these same 2 years (N = 4863 and N = 4777, respectively). The average daily census on all services was 1012 patients.

Some patients on all 3 services are co‐managed with house staff, who are responsible for writing physician orders. Control cohort patients were cared for by a mix of private attendings (approximately 75%) or hospitalists (25%), and in contradistinction to MACE patients, their typical care did not include daily interdisciplinary team rounds, a nurse coordinator, or geriatrics fellow. Social work and case management were unit‐ as opposed to team‐based. Care on the ACE unit‐based service differed from care for matched control patients by having daily interdisciplinary team rounds, a prepared environment, and nursing‐led protocols for the patients on the ACE unit.

Because the ACE unit‐based service admitted both patients who were and were not cared for in our ambulatory practice, while the MACE service admitted only patients cared for in the ambulatory practice, we deleted from the study sample the patients who did not have a visit to our outpatient practice before the index hospitalization. This allowed us to isolate the effect of the model of care itself as opposed to the effect of simply changing the patient base for admissions. We then merged the files with the hospital's administrative database and electronic billing system to obtain demographic and claims data.

Additional demographic data were obtained through chart review of the MACE patients during year 1. The chart review process was standardized using a data abstraction instrument and by determining inter‐rater reliability of the individual data abstractors (comprised of author B.K. and 4 MACE team members).

Costs were assigned to individual admissions by the hospital's cost reporting system and include a combination of traceable costs (such as imaging, laboratory, and pharmacy) and applied costs (nursing; allocated based on geographic location in the hospital) to arrive at direct and total costs.

We made 3 distinct comparisons of operational and quality outcomes using the above 5 groups, first comparing patients cared for on our traditional ACE unit‐based service to those cared for on the MACE service, and second and third comparing patients on the MACE service to propensity score‐matched controls during the first and second year of operations. Specifically, we hypothesized that the MACE service would be associated with reduced LOS, costs, and readmission rates compared with the ACE unit‐based service and the matched control groups. We used multivariate logistic regression to estimate the association of binary quality outcomes (mortality during the hospital stay, 7‐ and 30‐day readmission rates) with the existence of MACE while adjusting for confounding variables which included patient demographic and clinical characteristics such as age, gender, race, total number of comorbidities (calculated by Elixhauser method that includes 30 categories of comorbid illnesses identified by secondary diagnosis codes and discharge diagnosis‐related groups [DRGs]).7 We considered the clustering effect due to the same attending physician into the model as well. While adjusting for the same covariates, we used generalized linear models with a gamma distribution and log link to estimate the association of continuous variables (costs and LOS) with the existence of MACE.

The same statistical methods were applied to the second and third comparisons between patients cared for on the MACE and the propensity score‐matched cohorts for the first and second year of the MACE service. First, 2 control cohorts (N = 6148 and 5803 of our hospital discharges from July 1, 2007 to June 30, 2008, and July 1, 2008 to June 30, 2009, respectively, with age > 64 and with the identical DRG and All Patient Refined DRG (APR DRG) Severity of Illness (SOI) score as those of the MACE groups were obtained from our hospital's administrative database to reduce the selection bias. Then, 4863 patients within the first cohort (N = 6148) and 4777 patients within the second cohort (N = 5,803) with the closest propensity score were matched to 545 of 556 MACE patients and 494 of 501 MACE patients, respectively, in which the logit of their propensity score was within 0.02 standard deviations of the logit of the MACE patient's score.

Propensity scores were determined by logistic regression on whether patients were admitted to the MACE. The covariates for the propensity model were the same as the previously stated adjusting variables. Usual care patients' data were weighted to account for the one‐to‐many propensity score‐matching algorithm.

We similarly conducted a post hoc analysis of MACE compared with a subgroup control cohort of patients cared for by medicine hospitalists in year 1 (N = 1175) and year 2 (N = 1564), with age > 64 and with the identical DRG and APR DRG SOI as those of the MACE group. We then matched 1012 of the 1175 discharges with the closest propensity score to 389 of the 411 MACE discharges who were cared for by 1 of the 4 geriatric medicine hospitalists in year 1 and 1308 of the 1564 discharges to 471 of the 501 MACE discharges in year 2, in which the logit of their propensity score was within 0.02 standard deviations of the logit of the MACE patient's score, using the same covariates described above.

All analyses were done using Stata software, version 9.2 (StataCorp LP, College Station, TX). This project was exempted by the Institutional Review Board at Mount Sinai School of Medicine, New York, New York.

RESULTS

Table 2 presents the characteristics of the study subjects in all 5 groups. Patients cared for on the ACE unit‐based service and the MACE service in years 1 and 2 were very similar, with a mean age of 82.6, 83.2, and 83.6 years; 74.4%, 75.9%, and 76.7% were female; and mean Elixhauser comorbidity scores were 3.4, 3.3, and 3.5, respectively. Patients in the 2 matched control groups were likewise very similar to those in the matched MACE groups with regard to all demographic variables.

Chart review of the year 1 MACE discharges revealed that 70% spoke English as their primary language and 46% had cognitive impairment. Most lived at home alone (49%) or with family members (41%) while receiving some paid caregiver help (59%). The remaining 10% were admitted from either an assisted living facility (5%) or subacute rehabilitation (5%). Only 12% were wheelchair or bed‐bound, while 21% ambulated without and 67% with an assistive device. Their functional status was limited, with 58% dependent for both ADLs and IADLs, 22% dependent for IADLs only, and 20% independent in both. They had relatively high prescription medication burdens, with 10% taking 05, 34% taking 610, 38% taking 1115, and 18% taking >15 medications.

Patients cared for by the MACE service had an adjusted 2.1 days shorter LOS (P 0.001) when compared with patients cared for on the ACE unit service. Additionally, there was a net savings of $2872 in total costs per hospitalization (P = 0.002), $1094 in direct costs (P = 0.016), $849 in nursing costs (P 0.001), and $237 in pharmacy costs (P = 0.002). Imaging and laboratory costs between the 2 groups were not statistically different. There was no significant differences in in‐hospital mortality, 7‐day, 30‐day, or 90‐day readmission rates between the 2 groups (Table 3).

There was no difference in LOS between the MACE patients during the first year of service compared with propensity score‐matched control patients (5.8 vs 6.5 days). There was, however, a net savings of $2453 in total costs per hospitalization (P 0.001), $842 (P = 0.03) in direct costs, $393 in nursing costs (P = 0.026), and $39 in laboratory costs (P = 0.029). Imaging and pharmacy costs between the 2 groups were not statistically different. There was no significant differences in in‐hospital mortality, 7‐day or 30‐day readmission rates between the 2 groups. However, the 90‐day readmission rate was higher in MACE patients (Table 3).

During the second year of the MACE service, however, there was a significant reduction in LOS of 1.6 days (P 0.001), a net savings of $4943 in total costs per hospitalization (P 0.001), $2081 (P 0.001) in direct costs, $937 in nursing costs (P 0.001), $68 in laboratory costs (P 0.001), and $223 in pharmacy costs (P = 0.03). There were no significant differences in imaging costs, in‐hospital mortality, and 7‐day, 30‐day, or 90‐day readmission rates between the 2 groups (Table 3).

A subgroup analysis of the first and second year comparisons including only those patients in the control groups cared for by medicine hospitalists demonstrated reductions in the MACE in total cost in year 1 and LOS, mortality, total, and nursing costs in year 2. However, in year 1, the 30‐day and 90‐day readmission rates were increased in the MACE compared with the control group (Table 4).

We found no differences in a separate post hoc subgroup analysis assessing whether a 3‐month nurse coordinator's leave of absence during year 1 affected year 1 results. The service size was unaffected by her absence, and all patients continued to receive daily visits by the attending and fellow. During this time, other team members took over many of the nurse coordinator roles, except for the postdischarge phone calls.

DISCUSSION

Older adults constitute a disproportionate share of hospital admissions and hospital days. They typically have multiple comorbid conditions, higher rates of cognitive impairment and functional dependence, and complex social situations that all increase their risk of adverse outcomes. Current efforts for national healthcare reform focus on the combined economic and quality imperatives to improve the care of hospitalized older adults. Given the increasing representation of this fastest growing segment of the population in the acute care setting, the geographical unit‐based model for care delivery is untenable in many circumstances. Therefore, we developed a mobile ACE service in an effort to provide the geriatric‐focused acute care found on ACE units to older adults admitted to any medical unit in the hospital.

Our study compared operational and quality outcomes for older patients cared for by our mobile ACE service to those cared for on the unit‐based ACE service and other general medical services. We found a significant reduction in both LOS and costs in all 3 comparisons, except for LOS during the first year of the mobile ACE service. This heightened efficiency was not associated with changes in the quality measures of in‐hospital mortality and 7‐ and 30‐day readmission rates, though the 90‐day readmission rate was slightly higher for the MACE in year 1.

The adjusted total cost savings per admission in years 1 and 2 of approximately $2400 ($12,764 vs $10,311) and $4900 ($15,636 vs $10,693), respectively, translate into an overall annual savings of roughly $1,200,000 (500 patients $2400/patient) in year 1 and $2,450,000 (500 patients $4,900/patient) in year 2. The only relevant cost of the MACE service model compared with the comparison groups is the nurse coordinator salary and benefits, which are paid for by the hospital (as job responsibilities include participation in nursing department quality improvement projects and nursing education) and would not meaningfully offset these savings. The team social worker is a re‐allocation of existing hospital resources, whose salary line is likewise paid for by the hospital.

Our study has several important limitations. First, we lack data on readmissions to other hospitals. Our readmission rates are high compared with the national 19.6% 30‐day Medicare readmission rate cited in a recent study, and we failed to show significant reductions in in‐hospital mortality or 7‐ or 30‐day readmission rates.10 This lack of benefit may be related to control group patients, some of whom receive their community care outside of our institution, being more likely to be readmitted to other hospitals compared with our MACE patients, who were all receiving their ambulatory care in our associated faculty practice. In addition, the high readmission rate on the MACE service may be driven by a relatively small number of patients who are frequently admitted. For example, of the 363 unique MACE patients from year 2, 22 had 3 and 11 had 4 or 5 admissions. We are currently evaluating these 33 patients who accounted for 22% of the admissions to better understand the causes.

A second limitation of the study is selection bias. While patients were very well‐matched through propensity scoring and had identical DRG and DRG‐SOI levels (the latter having been demonstrated in a previous study's regression analysis to be the leading correlate of LOS and cost),9 there may be unaccounted for differences between the patients cared for on the MACE and in the control group. A third limitation is the external validity of our study, which took place in a single large academic medical center in New York City. While the MACE model may very well be readily adaptable elsewhere, numerous studies have demonstrated wide variation in medical practice patterns and healthcare use which may influence the exportability of the model.11, 12 However, our LOS of 5.8 and 5.6 days in years 1 and 2 of the MACE service, respectively, are similar to national data of 5.6 days for hospitalized adults >74 years of age.13

Benefits in cost and LOS reductions may be, in part, due to the hospitalist nature of the model as hospital medicine literature has demonstrated similar reductions for Medicare patients of approximately $1000 and 0.5 days per admission.8, 9 Our findings support this hypothesis as the LOS reduction was not present during the first year of our MACE service during which the hospitalist model was not fully implemented. During this transition phase from the unit‐based ACE to the mobile ACE service, there were 4 physicians who covered more than 75% of on‐service time (10 of the 13 annual 4‐week rotations), while the remaining 25% was covered by 3 physicians (each working 1 block). The following year (July 2008 to June 2009), during which an LOS reduction was demonstrated, a full geriatric medicine hospitalist model was in effect, with patients on the MACE service cared for 100% of the time (excluding weekends) by 1 of 4 geriatric medicine hospitalists. By comparison, 22% and 29% of control group patients were cared for by medicine hospitalists during years 1 and 2, respectively. In addition to this transition to a hospitalist model, there may have been other undefined service improvements over the first year which contributed to the LOS and total cost reductions achieved in year 2 in the hospitalist subgroup analysis. Likewise, the increased 90‐day readmission rates seen in year 1 but not in year 2 in both the main and hospitalist subgroup analyses may be related to MACE service improvements over time. A more vigorous proactive intervention beyond the follow‐up phone call is likely needed to impact 90‐day readmissions.

LOS reductions may also have been related to the interdisciplinary team‐based approach in which a need for family meetings to address goals of care or assess and attempt to resolve complex family/living situations was identified early in the course of hospitalization. Likewise, in New York State, the application process for discharge to a postacute care setting begins with the completion of a Patient Review Instrument (PRI), which contains detailed information on the patient's physical, medical, and cognitive status. The MACE model circumvents the traditional case manager's role of completing the PRI by having the MACE nurse coordinator trained and certified to do so. The daily or twice daily MACE team meeting may have enabled more timely initiation of this early step in the discharge process for these patients, ultimately resulting in a reduced LOS.

An important concern this study is not able to address is whether LOS reductions are achieved at a price of impaired functional status. A prospective longitudinal study on the outcomes of patients cared for by a MACE service that includes detailed assessments of functional status based upon information gathered during admission and postdischarge during follow‐up phone calls is needed to properly evaluate this possibility.

Given the lack of wide‐spread adoption of the traditional ACE unit‐based model of care and its inherent limitations in the setting of high occupancy rates, a mobile ACE service may prove useful in providing high quality clinical care with reduced LOS and costs. This team‐based, as opposed to unit‐based, approach benefits from having low entry costs, as hospital administration can re‐allocate existing resources to fit the model and avoid costly capital investments in specialized unit design and outfitting. Further research should include metrics on functional status, all‐hospital readmission rates, and patient/caregiver satisfaction to better assess the feasibility of this acute care model.

The traditional acute care for the elderly (ACE) unit has demonstrated improved functional outcomes without increased costs or changes in length of stay (LOS).15 It is, however, limited in scope to only those patients cared for on a fixed geographical unit. This structural limitation is of increasing relevance in times of high hospital bed occupancy rates, as during such times, many appropriate older patients are admitted elsewhere. In our experience with a traditional ACE unit‐based model, only 52% of our geriatrics practice patients were admitted to an ACE unit bed, while the remainder were admitted to various medical units throughout the hospital. We therefore abandoned our traditional unit‐based ACE service in July 2007 in favor of a mobile ACE (MACE) service, bringing the interdisciplinary, patient‐centered team approach to our hospitalized older adult patients admitted throughout the hospital.

The purpose of this study is to compare the operational and quality outcomes for patients cared for on the MACE service to those cared for on a unit‐based ACE service and matched controls cared for on other general medical services. We hypothesized that the MACE service would be associated with lower lengths of stay, reduced costs, and decreased rehospitalization rates.

METHODS

The MACE team was composed of a geriatrician‐hospitalist, geriatric medicine fellow, social worker, and nurse coordinator. The geriatric medicine attending on the MACE service was in the hospital providing patient care during regular working hours from Monday through Friday, while the weekends were covered by a rotating group of all geriatric medicine faculty. During the first and second years of MACE, there were 7 and 4 attendings, respectively; all fellowship‐trained geriatricians. Three of the 4 geriatric medicine hospitalists during year 2 had been in practice between 1 and 3 years postfellowship and also had training in palliative medicine, although were not board‐certified in the latter. The fourth hospitalist had been in practice for 5 years postfellowship. The interdisciplinary team met daily to discuss the care of all patients and used a transitional care model based on The Care Transitions Program⁶ adapted to our institution, with a focus on reducing the risks of hazards of hospitalization. Care coordination with the outpatient practice, early family meetings, discharge planning, patient and caregiver education, and postdischarge follow‐up phone calls were some of the key hallmarks of the service (Table 1).

We conducted a retrospective cohort study with propensity‐score matching in an urban academic medical center. Study subjects comprised 5 distinct groups. First were community‐dwelling older adults cared for at our outpatient geriatrics ambulatory practice who were discharged from our traditional ACE unit‐based acute care service at the Mount Sinai Hospital from July 1, 2006 through June 30, 2007 (N = 450). Second and third were patients from the same practice discharged from our MACE service during the first 2 years of operation (N = 556 from July 1, 2007 through June 30, 2008, and N = 501 from July 1, 2008 through June 30, 2009). Fourth and fifth were control cohorts of hospitalized older adults discharged from other medical services at the Mount Sinai Hospital during these same 2 years (N = 4863 and N = 4777, respectively). The average daily census on all services was 1012 patients.

Some patients on all 3 services are co‐managed with house staff, who are responsible for writing physician orders. Control cohort patients were cared for by a mix of private attendings (approximately 75%) or hospitalists (25%), and in contradistinction to MACE patients, their typical care did not include daily interdisciplinary team rounds, a nurse coordinator, or geriatrics fellow. Social work and case management were unit‐ as opposed to team‐based. Care on the ACE unit‐based service differed from care for matched control patients by having daily interdisciplinary team rounds, a prepared environment, and nursing‐led protocols for the patients on the ACE unit.

Because the ACE unit‐based service admitted both patients who were and were not cared for in our ambulatory practice, while the MACE service admitted only patients cared for in the ambulatory practice, we deleted from the study sample the patients who did not have a visit to our outpatient practice before the index hospitalization. This allowed us to isolate the effect of the model of care itself as opposed to the effect of simply changing the patient base for admissions. We then merged the files with the hospital's administrative database and electronic billing system to obtain demographic and claims data.

Additional demographic data were obtained through chart review of the MACE patients during year 1. The chart review process was standardized using a data abstraction instrument and by determining inter‐rater reliability of the individual data abstractors (comprised of author B.K. and 4 MACE team members).

Costs were assigned to individual admissions by the hospital's cost reporting system and include a combination of traceable costs (such as imaging, laboratory, and pharmacy) and applied costs (nursing; allocated based on geographic location in the hospital) to arrive at direct and total costs.

We made 3 distinct comparisons of operational and quality outcomes using the above 5 groups, first comparing patients cared for on our traditional ACE unit‐based service to those cared for on the MACE service, and second and third comparing patients on the MACE service to propensity score‐matched controls during the first and second year of operations. Specifically, we hypothesized that the MACE service would be associated with reduced LOS, costs, and readmission rates compared with the ACE unit‐based service and the matched control groups. We used multivariate logistic regression to estimate the association of binary quality outcomes (mortality during the hospital stay, 7‐ and 30‐day readmission rates) with the existence of MACE while adjusting for confounding variables which included patient demographic and clinical characteristics such as age, gender, race, total number of comorbidities (calculated by Elixhauser method that includes 30 categories of comorbid illnesses identified by secondary diagnosis codes and discharge diagnosis‐related groups [DRGs]).7 We considered the clustering effect due to the same attending physician into the model as well. While adjusting for the same covariates, we used generalized linear models with a gamma distribution and log link to estimate the association of continuous variables (costs and LOS) with the existence of MACE.

The same statistical methods were applied to the second and third comparisons between patients cared for on the MACE and the propensity score‐matched cohorts for the first and second year of the MACE service. First, 2 control cohorts (N = 6148 and 5803 of our hospital discharges from July 1, 2007 to June 30, 2008, and July 1, 2008 to June 30, 2009, respectively, with age > 64 and with the identical DRG and All Patient Refined DRG (APR DRG) Severity of Illness (SOI) score as those of the MACE groups were obtained from our hospital's administrative database to reduce the selection bias. Then, 4863 patients within the first cohort (N = 6148) and 4777 patients within the second cohort (N = 5,803) with the closest propensity score were matched to 545 of 556 MACE patients and 494 of 501 MACE patients, respectively, in which the logit of their propensity score was within 0.02 standard deviations of the logit of the MACE patient's score.

Propensity scores were determined by logistic regression on whether patients were admitted to the MACE. The covariates for the propensity model were the same as the previously stated adjusting variables. Usual care patients' data were weighted to account for the one‐to‐many propensity score‐matching algorithm.

We similarly conducted a post hoc analysis of MACE compared with a subgroup control cohort of patients cared for by medicine hospitalists in year 1 (N = 1175) and year 2 (N = 1564), with age > 64 and with the identical DRG and APR DRG SOI as those of the MACE group. We then matched 1012 of the 1175 discharges with the closest propensity score to 389 of the 411 MACE discharges who were cared for by 1 of the 4 geriatric medicine hospitalists in year 1 and 1308 of the 1564 discharges to 471 of the 501 MACE discharges in year 2, in which the logit of their propensity score was within 0.02 standard deviations of the logit of the MACE patient's score, using the same covariates described above.

All analyses were done using Stata software, version 9.2 (StataCorp LP, College Station, TX). This project was exempted by the Institutional Review Board at Mount Sinai School of Medicine, New York, New York.

RESULTS

Table 2 presents the characteristics of the study subjects in all 5 groups. Patients cared for on the ACE unit‐based service and the MACE service in years 1 and 2 were very similar, with a mean age of 82.6, 83.2, and 83.6 years; 74.4%, 75.9%, and 76.7% were female; and mean Elixhauser comorbidity scores were 3.4, 3.3, and 3.5, respectively. Patients in the 2 matched control groups were likewise very similar to those in the matched MACE groups with regard to all demographic variables.

Chart review of the year 1 MACE discharges revealed that 70% spoke English as their primary language and 46% had cognitive impairment. Most lived at home alone (49%) or with family members (41%) while receiving some paid caregiver help (59%). The remaining 10% were admitted from either an assisted living facility (5%) or subacute rehabilitation (5%). Only 12% were wheelchair or bed‐bound, while 21% ambulated without and 67% with an assistive device. Their functional status was limited, with 58% dependent for both ADLs and IADLs, 22% dependent for IADLs only, and 20% independent in both. They had relatively high prescription medication burdens, with 10% taking 05, 34% taking 610, 38% taking 1115, and 18% taking >15 medications.

Patients cared for by the MACE service had an adjusted 2.1 days shorter LOS (P 0.001) when compared with patients cared for on the ACE unit service. Additionally, there was a net savings of $2872 in total costs per hospitalization (P = 0.002), $1094 in direct costs (P = 0.016), $849 in nursing costs (P 0.001), and $237 in pharmacy costs (P = 0.002). Imaging and laboratory costs between the 2 groups were not statistically different. There was no significant differences in in‐hospital mortality, 7‐day, 30‐day, or 90‐day readmission rates between the 2 groups (Table 3).

There was no difference in LOS between the MACE patients during the first year of service compared with propensity score‐matched control patients (5.8 vs 6.5 days). There was, however, a net savings of $2453 in total costs per hospitalization (P 0.001), $842 (P = 0.03) in direct costs, $393 in nursing costs (P = 0.026), and $39 in laboratory costs (P = 0.029). Imaging and pharmacy costs between the 2 groups were not statistically different. There was no significant differences in in‐hospital mortality, 7‐day or 30‐day readmission rates between the 2 groups. However, the 90‐day readmission rate was higher in MACE patients (Table 3).

During the second year of the MACE service, however, there was a significant reduction in LOS of 1.6 days (P 0.001), a net savings of $4943 in total costs per hospitalization (P 0.001), $2081 (P 0.001) in direct costs, $937 in nursing costs (P 0.001), $68 in laboratory costs (P 0.001), and $223 in pharmacy costs (P = 0.03). There were no significant differences in imaging costs, in‐hospital mortality, and 7‐day, 30‐day, or 90‐day readmission rates between the 2 groups (Table 3).

A subgroup analysis of the first and second year comparisons including only those patients in the control groups cared for by medicine hospitalists demonstrated reductions in the MACE in total cost in year 1 and LOS, mortality, total, and nursing costs in year 2. However, in year 1, the 30‐day and 90‐day readmission rates were increased in the MACE compared with the control group (Table 4).

We found no differences in a separate post hoc subgroup analysis assessing whether a 3‐month nurse coordinator's leave of absence during year 1 affected year 1 results. The service size was unaffected by her absence, and all patients continued to receive daily visits by the attending and fellow. During this time, other team members took over many of the nurse coordinator roles, except for the postdischarge phone calls.

DISCUSSION

Older adults constitute a disproportionate share of hospital admissions and hospital days. They typically have multiple comorbid conditions, higher rates of cognitive impairment and functional dependence, and complex social situations that all increase their risk of adverse outcomes. Current efforts for national healthcare reform focus on the combined economic and quality imperatives to improve the care of hospitalized older adults. Given the increasing representation of this fastest growing segment of the population in the acute care setting, the geographical unit‐based model for care delivery is untenable in many circumstances. Therefore, we developed a mobile ACE service in an effort to provide the geriatric‐focused acute care found on ACE units to older adults admitted to any medical unit in the hospital.

Our study compared operational and quality outcomes for older patients cared for by our mobile ACE service to those cared for on the unit‐based ACE service and other general medical services. We found a significant reduction in both LOS and costs in all 3 comparisons, except for LOS during the first year of the mobile ACE service. This heightened efficiency was not associated with changes in the quality measures of in‐hospital mortality and 7‐ and 30‐day readmission rates, though the 90‐day readmission rate was slightly higher for the MACE in year 1.

The adjusted total cost savings per admission in years 1 and 2 of approximately $2400 ($12,764 vs $10,311) and $4900 ($15,636 vs $10,693), respectively, translate into an overall annual savings of roughly $1,200,000 (500 patients $2400/patient) in year 1 and $2,450,000 (500 patients $4,900/patient) in year 2. The only relevant cost of the MACE service model compared with the comparison groups is the nurse coordinator salary and benefits, which are paid for by the hospital (as job responsibilities include participation in nursing department quality improvement projects and nursing education) and would not meaningfully offset these savings. The team social worker is a re‐allocation of existing hospital resources, whose salary line is likewise paid for by the hospital.

Our study has several important limitations. First, we lack data on readmissions to other hospitals. Our readmission rates are high compared with the national 19.6% 30‐day Medicare readmission rate cited in a recent study, and we failed to show significant reductions in in‐hospital mortality or 7‐ or 30‐day readmission rates.10 This lack of benefit may be related to control group patients, some of whom receive their community care outside of our institution, being more likely to be readmitted to other hospitals compared with our MACE patients, who were all receiving their ambulatory care in our associated faculty practice. In addition, the high readmission rate on the MACE service may be driven by a relatively small number of patients who are frequently admitted. For example, of the 363 unique MACE patients from year 2, 22 had 3 and 11 had 4 or 5 admissions. We are currently evaluating these 33 patients who accounted for 22% of the admissions to better understand the causes.

A second limitation of the study is selection bias. While patients were very well‐matched through propensity scoring and had identical DRG and DRG‐SOI levels (the latter having been demonstrated in a previous study's regression analysis to be the leading correlate of LOS and cost),9 there may be unaccounted for differences between the patients cared for on the MACE and in the control group. A third limitation is the external validity of our study, which took place in a single large academic medical center in New York City. While the MACE model may very well be readily adaptable elsewhere, numerous studies have demonstrated wide variation in medical practice patterns and healthcare use which may influence the exportability of the model.11, 12 However, our LOS of 5.8 and 5.6 days in years 1 and 2 of the MACE service, respectively, are similar to national data of 5.6 days for hospitalized adults >74 years of age.13

Benefits in cost and LOS reductions may be, in part, due to the hospitalist nature of the model as hospital medicine literature has demonstrated similar reductions for Medicare patients of approximately $1000 and 0.5 days per admission.8, 9 Our findings support this hypothesis as the LOS reduction was not present during the first year of our MACE service during which the hospitalist model was not fully implemented. During this transition phase from the unit‐based ACE to the mobile ACE service, there were 4 physicians who covered more than 75% of on‐service time (10 of the 13 annual 4‐week rotations), while the remaining 25% was covered by 3 physicians (each working 1 block). The following year (July 2008 to June 2009), during which an LOS reduction was demonstrated, a full geriatric medicine hospitalist model was in effect, with patients on the MACE service cared for 100% of the time (excluding weekends) by 1 of 4 geriatric medicine hospitalists. By comparison, 22% and 29% of control group patients were cared for by medicine hospitalists during years 1 and 2, respectively. In addition to this transition to a hospitalist model, there may have been other undefined service improvements over the first year which contributed to the LOS and total cost reductions achieved in year 2 in the hospitalist subgroup analysis. Likewise, the increased 90‐day readmission rates seen in year 1 but not in year 2 in both the main and hospitalist subgroup analyses may be related to MACE service improvements over time. A more vigorous proactive intervention beyond the follow‐up phone call is likely needed to impact 90‐day readmissions.

LOS reductions may also have been related to the interdisciplinary team‐based approach in which a need for family meetings to address goals of care or assess and attempt to resolve complex family/living situations was identified early in the course of hospitalization. Likewise, in New York State, the application process for discharge to a postacute care setting begins with the completion of a Patient Review Instrument (PRI), which contains detailed information on the patient's physical, medical, and cognitive status. The MACE model circumvents the traditional case manager's role of completing the PRI by having the MACE nurse coordinator trained and certified to do so. The daily or twice daily MACE team meeting may have enabled more timely initiation of this early step in the discharge process for these patients, ultimately resulting in a reduced LOS.

An important concern this study is not able to address is whether LOS reductions are achieved at a price of impaired functional status. A prospective longitudinal study on the outcomes of patients cared for by a MACE service that includes detailed assessments of functional status based upon information gathered during admission and postdischarge during follow‐up phone calls is needed to properly evaluate this possibility.

Given the lack of wide‐spread adoption of the traditional ACE unit‐based model of care and its inherent limitations in the setting of high occupancy rates, a mobile ACE service may prove useful in providing high quality clinical care with reduced LOS and costs. This team‐based, as opposed to unit‐based, approach benefits from having low entry costs, as hospital administration can re‐allocate existing resources to fit the model and avoid costly capital investments in specialized unit design and outfitting. Further research should include metrics on functional status, all‐hospital readmission rates, and patient/caregiver satisfaction to better assess the feasibility of this acute care model.