An iatrogenic metabolic encephalopathy in a nonagenarian: The dilemma of a critical miss as a possible social dismissal.

Here we posit for discussion the example of a reversible metabolic encephalopthy in a very elderly male that was missed clinically. A metabolic encephalopathy in extrememly elderly patients may be confused with delerium or inattention. A reversible cause of cognative dysfunction in the aged may be missed by practitioners because the aged may be assumed to have some level of impaired cognition; this may lead to a "social dismissal" of mental status changes. We highlight the need for engaged physicians in the care of the aged and vigilance against a professional bias toward the elderly patient that is dismissive.

INTRODUCTION

Metabolic encephalopathy (ME) can be described as an interaction between hypoxia/anoxia, hepatic, renal, septic, immune-mediated, and electrolyte/endocrine disturbances,[1] and is frequently confused with delirium,[2] especially asociated with a rapidly progressive dementia.[3] In the nonagenarians, an acute loss of cognitive dysfunction may precipitate a less aggressive medical intervention, and can potentially contribute to missing a potentially simple, easy-to-treat diagnosis. As we report here, this may appear as a “social dismissal” of the aged patient.[45]

CASE REPORT

A 93-year-old male, 70 kg, 165 cm, was admitted to (the first of three hospitals) with a diagnosis of congestive heart failure attributed to right ventricular dysfunction. He required a walker for ambulation. He had a past medical history of a coronary artery disease, atrial fibrillation, mitral regurgitation, aortic stenosis, diverticular bleeding, hypertension, advanced chronic kidney disease, gout (remote), and nonAlzheimer's dementia. His surgical history included coronary artery bypass grafting with mitral valve and aortic valve replacement (tissue valves). His medications were donepezil for dementia, calcium carbonate, potassum chloride, isosorbide mononitrate, metamucil, pantoprazole, diltiazem, hydralazine, and bumetanide.

The laboratory evaluation demonstrated: Sodium 140 mmol/L, potassium 4.0 mmol/L, chloride 95 mmol/L, serum bicarbonate 36 mmol/L, phosphorus 3.4 mg/dl, magnesium 2.2 mg/dL, glucose 108 mg/dL, blood urea nitrogen (BUN) 73 mg/dL, creatinine 2.13 mg/dL, glomerular filtration rate (GFR) 29 mL/min, occult blood negative, total protein 6.3 g/dL, albumin 3.8 g/dL, thyroid function tests were normal, hemoglobin 9.7 g/dL, hematocrit 29.3%, white blood cell count 4.6 K/μL, and platelets 90 K/μL.

Physical examination revealed bilateral pulmonary rales, tachypnea, pedal edema, and rate-controlled atrial fibrillation (confirmed by electrocardiogram). Chest roentgenogram showed bilateral pleural effusions and pulmonary edema.

A furosemide infusion promoted a 6 kg loss in 5 days; tachypnea, pedal edema, pulmonary edema, and pleural effusions improved. Concurrently he complained of leg pain and received tramadol 50 mg every 8 hours. His cognitive function worsened over 72 hours (days 3-5 of diuresis). He also became incontinent, needed skilled nursing care, and was transferred to a covalesent facility where he was difficult to arouse upon arrival. He had lost intravenous access and none was started. No laboratory studies were drawn. The staff suggested that the patient be made “comfort care” only. The next morning his condition remained unchanged. The family expressed concern and transferred the patient to a third institution.

Subsequent examination revealed a Glasgow coma scale of 10, mild bilateral rales, rate controlled atrial fibrillation, no pretibial edema, and an edematous left foot with an erythematous, warm great toe. Urine output was diminished. Laboratory examination revealed a BUN of 81 mg/dL (GFR < 30 mL/min), potassium, sodium, and chloride were normal, and serum bicarbonate 43 mmol/L, and arterial blood gas was pH of 7.37, PaCO2 65, and PaO2 of 90 (2 liters nasal cannula). His uric acid level was 450 μmol/L.

He received crystalloid fluids at 100 mL/hour for 24 hours, and bilevel noninvasive mechanical ventilation 12/4 cm H2O. He subsequently improved over 36 hours. His ME from a compensated metabolic alkalosis with hypercapnea was corrected, and urine output improved. He could now converse, feed himself, and walk 50 feet with his walker.

DISCUSSION

This patient had developed a ME from a metabolic alkalosis secondary to aggressive diuresis that led to an unrecognized compensated hypercapneic state complicated by tramadol 50 mg every 8 hours for leg pain (undiagnosed gout) in the face of a very low GFR. His advanced age and history of dementia may have led to his “social dismissal” by the treating medical staff.

The patient's chronic renal insufficiency was exacerbated by the furosemide drip intended to relieve his pulmonary edema. Although successful, the aggressive diuresis caused volume contracture (metabolic alkalosis), compensatory hypercapnea, and hyperuricemia. His previous history of gout left him vulnerable to a diuresis-induced relapse. Hunter et al. found that the odds ratio for recurrent gout attacks from all diuretic use over 48 hours was 3.6, with odds ratios for thiazide and loop diuretics being 3.2 and 3.8, respectively.[6] Although tramadol hydrochloride generally causes less repiratory depression than morphine, it is a centrally acting synthetic analgesic that may cause sedation and must be used cautiously in patients at risk for respiratory depression dose adjustment is required for GFR < 30 mL/min.[7] It binds to mu opioid receptors and weakly inhibits norepinephrine/serotonin reuptake, producing analgesia. It is metabolized in the liver through CYP450 and has an active metabolite (M1) that is excreted through the kidneys. Its half-life is 6.3 hours and that of its metabolite is 7.4 hours; 4 hours of dialysis will remove < 10% of an administered dose.[8910]

While the patient's age, his premorbid state, and the circumstances of his recent medical hospitalization led to the impression that his condition was one from which he was unlikely to meaningfully recover, a more thorough investigation of the simpler causes of his mental status change would have better served this patient.

CONCLUSION

The aged in our society are increasing in numbers and longevity. A more balanced diagnostic and therapeutic approach to the elderly, akin to that toward younger patients, needs to evolve. Besides the concerns regarding the differential diagnosis of a change in mental status/ME, important social issues come into focus: (a) The dismissal of the physical and mental problems of the aged citizen is an unacceptable option; (b) patients may fare better if a dedicated primary physician manages their care with the advice of consultants, avoiding excessive specialist involvement without “central coordination”; (c) the lack of critical care skills and critical thinking often coexist among highly educated medical staff; (d) there is a need for second opinions and this should be considered an acceptable practice; and (e) family interaction with the medical/nursing staff regarding their loved one is frequently helpful, and must be recognized and accepted as such. We must be vigilant against a professional mindset of age bias that inherently assumes that the elderly are generally a burden to society's economic and healthcare system, thus overlooking simple solutions to seemingly terminal or complex problems.