Psychosomatics 48:352-354, July-August 2007
doi: 10.1176/appi.psy.48.4.352
© 2007 Academy of Psychosomatic Medicine
Pancreatic Encephalopathy With Prolonged Delirium
James A. Bourgeois, O.D., M.D., and
David Fakhri, D.O.
Received October 19, 2005; revised December 29, 2005; accepted January 9, 2006. From the Department of Psychiatry and Behavioral Sciences, University of California, Davis Medical Center. Send correspondence and reprint requests to James A. Bourgeois, O.D., M.D., Department of Psychiatry and Behavioral Sciences, University of California, Davis Medical Center, 2230 Stockton Blvd., Sacramento CA 95817. e-mail: james.bourgeois{at}ucdmc.ucdavis.edu
© 2007 The Academy of Psychosomatic Medicine
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INTRODUCTION
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A 64-year-old white man presented with acute pancreatitis and delirium. He did not receive antipsychotics during a 15-day period of illness. He recovered with good cognitive functioning and no residual psychiatric symptoms.
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Case Report
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A 64-year-old white man presented with a 2-day history of severe, non-radiating, bilateral lower quadrant abdominal and flank pain, nausea, and vomiting. He had no history of alcoholism, gallstones, or hyperlipidemia, and medical history was otherwise unremarkable. Laboratory studies included a white blood count (WBC) of 17.3 k/mm3, amylase: 4,156 U/liter, lipase: 8,195 U/liter, LDH: 459 U/liter, triglycerides: 42 mg/dl, total bilirubin: 4.9 mg/dl, AST: 364 U/liter, ALT: 366 U/liter, and albumin: 4.1g/dl. CT scan demonstrated pancreatitis; ultrasound showed no evidence of gallstones. He was diagnosed with acute pancreatitis and transferred to a university medical center.
Upon arrival, his mental status exam revealed full alertness, with agitation, paranoid ideation, confusion, and disorientation. Laboratory studies included WBC: 17.6 k/mm3 (reference range: 4.5–11), amylase: 774 U/liter (30–140), lipase: 187 U/liter (13–51), LDH: 570 U/liter (90–200), triglycerides: 177 mg/dl (35–160), total bilirubin: 4.7 mg/dl (0.3–1.3), AST: 63 U/liter (15–43), ALT: 102 U/liter (6–63), albumin: 2.0 g/dl (3.2–4.6), glucose: 151 mg/dl (70–110), INR: 1.25 (0.75–1.19), ABG (arterial blood gases) pH: 7.35, pCO2: 48 mmHg, PO2: 68 mmHg, sodium: 148 meq/liter, potassium: 3.4 meq/liter, calcium: 7.6 mg/dl, and magnesium: 2.0 mg/dl. Chest X-ray revealed left pleural effusion. Blood and sputum cultures were negative.
He was kept NPO and received meropenem, folate, pantoprazole, insulin, and IV hydration. Because of continued agitation, he received the following IV drips: hydromorphone (Days 1–10), propofol (Days 3–5), lorazepam (Days 4–8), and morphine (Days 10–11). His initial psychosomatic medicine (PSM) consultation was on Day 3. At that point, he had had altered mental status for 3 days, including hallucinating his wife’s voice when she was not present, and paranoid ideations about threatening behavior of ICU nurses. Despite PSM service recommendations, antipsychotics were not used, because of the concern of the primary medical team that he would become more sedated.
Repeated CT on Day 3 showed a low-density area in the neck and body of the pancreas suspicious for pancreatitis with phlegmon. Amylase and lipase normalized by Day 4. An endoscopic ultrasound showed a hypoechoic fullness of the pancreatic head and neck. He was extubated on Day 9, but continued with altered mental status, including intermittent agitation, somnolence, and confusion. On Day 12, he was transferred to a medical ward. On repeat PSM examination, he was somnolent but arousable. He appeared depressed and confused. He denied psychotic symptoms, had limited understanding of why he was hospitalized, and requested discharge. Mini-Mental State Exam (MMSE) score was 9. On PSM examination on Day 14, he stated that he was hospitalized "because (of) my testestosterone (sic) gland." He continued to be perseverative and circumstantial; MMSE score was 6. MRI revealed a "punctuate focus of high signal in diffusion-weighted images, which may represent a small infarct in the posterior right frontal white matter." He was started on pancrealipase.
By Day 15, he was alert, and behaving appropriately. He could recall his spouse’s visit from the day before. He recalled psychotic symptoms he had experienced before hospitalization of "having artwork speak to him." MMSE was 20, with residual poor time-orientation, attention, and recall memory. On Day 16, he continued his improvement, with MMSE of 24. CT on Day 17 revealed a pancreatic pseudocyst and possible abscess in the pancreas. He was diagnosed with idiopathic necrotizing pancreatitis. When seen by PSM on Day 19, mental status had returned to baseline; MMSE was 28.
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Discussion
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Pancreatic encephalopathy, severe delirium in the context of pancreatitis, was initially described in 1941.1 Sharf and Bental described a 58-year-old woman with pancreatitis and "confusion" (that later deteriorated to akinetic mutism), which manifested 9 days after presentation.2 EEG revealed irregular background activity and slow focal theta and delta waves over the left fronto-parietal region. Weeks later, after treatment with the proteinase inhibitor aprotinin, mental status improved to near-baseline. The authors suggested that pancreatic enzymes were culpable in causing delirium.
Johnson and Tong3 reported on a 34-year-old man who died from pancreatic encephalopathy with agitation, after seizures, within several hours of presentation. Pathological study revealed a cerebral fat embolism. The authors felt that the pathophysiological mechanism was a pulmonary fat embolism, leading to hypoxia, with a possible additional role for cerebral fat metabolism.
Estrada et al.4 prospectively studied 17 cases of acute pancreatitis and found encephalopathy (with visual and auditory hallucinations and time- and place-disorientation) in 6 cases. They reported a direct relationship between pancreatic encephalopathy and increased CSF lipase. The neuropsychiatric, EEG, and CSF lipase abnormalities reversed within 10 days.
Sjaastad et al.5 reported relapsing pancreatitis until the patient’s death at age 46. In her last year, she exhibited fatigue, "giddiness," amnesia, poor concentration, and aphasia. CT scan revealed diffuse cortical atrophy. She had increased CSF and plasma amino acids, suggesting aberrant urea-cycle functioning.
Guardia et al.6 described acute pancreatitis with severe agitation and fatal multi-organ system failure in a 51-year-old woman. Pathology examination revealed petechial hemorrhages of the cerebrum, cerebellum, corpus callosum, basal ganglia, midbrain, pons, and medulla. The proposed mechanism of death was a cerebral fat embolism and pulmonary fat embolism, resulting in hypoxia.
Boon et al.7 reported on a 59-year-old man who developed acute pancreatitis and progressive cognitive impairment. CT scan showed cortical atrophy; EEG showed bilateral theta activity and intermittent delta activity. An MRI 3 weeks later revealed multiple small lesions in the white matter. Three weeks thereafter, his neuropsychiatric status had normalized.
Ruggieri et al.8 reported on a 43-year-old man who developed clouded consciousness, disorientation, auditory hallucinations, and, eventually, coma within 2 weeks of the onset of acute pancreatitis. CT scans and MRI were normal. Upon recovery from coma, he experienced disorientation, short attention span, amnesia, and aphasia, with persistent apathy. EEG revealed diffuse slowing with theta waves. A subsequent MRI revealed cortical and subcortical atrophy after a second episode.
Our case is consistent with the cases of pancreatic encephalopathy in the literature. Although the descriptions of mental status changes in other cases vary, they are consistent with the current phenomenology of delirium. Our patient had periods of both increased ("hyperactive" delirium) and decreased activity ("hypoactive" delirium); thus, his delirium episode was "mixed." The literature suggests several mechanisms for pancreatic encephalopathy; for example, CNS toxicity from pancreatic enzymes, increased CSF lipase, hypoxia from pulmonary fat emboli, CNS fat emboli, and aberrant urea-cycle metabolism.
Our patient had a long episode of delirium, which developed just before his hospitalization (when his amylase and lipase levels were at their peak) and persisted for 10 days after renormalization of the amylase and lipase. This suggests a mechanism beyond amylase/lipase CNS toxicity. His initial arterial blood gas analysis demonstrated hypoxia; however, his delirium continued for several days after extubation, suggesting that correction of respiratory status did not promptly reverse his delirium. MRI of the brain later in the course of hospitalization showed a focus of high signal intensity, possibly representing a small infarct, suggesting a possible role for cerebral fat embolism. Although delirium was observed before the use of sedatives, the various sedatives used in the first 11 days could have exacerbated the delirium. During these first 2 weeks, there were repeated attempts to lessen sedation, only to find the patient still prone to agitation.
PSM psychiatrists should consider a multifaceted approach to pancreatic encephalopathy. Early neuroimaging is indicated, even if it does not change management, because cases have shown cortical atrophy and/or focal CNS lesions. These may have prognostic significance; especially if the patient has recurrent pancreatic encephalopathy. Neuroimaging may reveal structural lesions that increase susceptibility to delirium. Regular monitoring of cognitive status and patience with a prolonged course of delirium are needed. Antipsychotics appear warranted, especially for psychosis and agitation, with monitoring for reemergence of delirium when they are tapered. Benzodiazepines and opioids should be minimized. Post-recovery explanation of delirium symptoms to the patient may assist with adjustment.
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REFERENCES
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- Rotermich NO, von Haam E: Pancreatic encephalopathy. J Clin Endocrin 1941; 1:872–881
- Sharf B, Bental E: Pancreatic encephalopathy. J Neurol Neurosurg Psychiatry 1971; 34:357–361[Abstract/Free Full Text]
- Johnson DA, Tong NT: Pancreatic encephalopathy. South Med J 1977; 70:165–167[Medline]
- Estrada RV, Moreno J, Martinez E, et al: Pancreatic encephalopathy. Acta Neurol Scandinav 1979; 59:135–139[Medline]
- Sjaastad O, Gjessing, Ritland S, et al: Chronic relapsing pancreatitis, encephalopathy with disturbances of consciousness, and CSF amino acid aberration. J Neurol 1979; 220:83–94[CrossRef][Medline]
- Guardia N, Bilbao JM, Murray D, et al: Fat embolism in acute pancreatitis. Arch Pathol Lab Med 1989; 113:503–506[Medline]
- Boon P, de Reuck J, Achten E, et al: Pancreatic encephalopathy: a case report and review of the literature. Clin Neurol Neurosurg 1991; 93:137–141[CrossRef][Medline]
- Ruggieri RM, Lupo I, Piccoli F: Pancreatic encephalopathy: a 7-year follow-up case report and review of the literature. Neurol Sci 2002; 23:203–205[CrossRef][Medline]
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INTRODUCTION
Case Report
