Acute Hypoglycemia Presenting as Acute Psychosis

Tanveer Padder MD, Aparna Udyawar MD, Nouman Azhar MD, Kamil Jaghab MD
From the Department of Psychiatry, Nassau University Medical Center, 2201 Hempstead Turnpike, East Meadow NY 11554 USA.

We are presenting a unique case of acute hypoglycemia presenting as acute psychosis with an unusual presentation creating a diagnostic dilemma. Medline search was done using the search words hypoglycemia and psychosis and to the best of our knowledge this is the first reported case of hypoglycemia presenting as acute psychosis. Unsuspected hypoglycemia may masquerade as neurologic, psychiatric, traumatic, or toxicologic disorders. Hypoglycemia has been misdiagnosed as cerebrovascular accident, transient ischemic attack, seizure disorder, brain tumor, narcolepsy, multiple sclerosis, psychosis, sympathomimetic drug ingestion, hysteria, and depression and also can masquerade as traumatic head injury with varying degrees of altered mentation, (1) as well as cardiac arrhythmia with bradycardia. (2) Our case provides a unique look at how a simple abnormality when overlooked can present as a difficult diagnostic challenge for both medicine and psychiatry services. Particular care should be exercised when dealing with psychiatric patients with these entities so that hypoglycemia is not missed. Significant medical harm to the patient and medicolegal risks for the emergency physician are issues to consider in cases involving misdiagnosis, incorrect therapy, and inappropriate disposition. (3)

Almost 7% patients presenting with altered mental status to the ED are in fact hypoglycemic. In addition to the diabetic patient, numerous other clinical scenarios may involve hypoglycemia, including toxicologic, infectious, psychiatric, and metabolic syndrome presentations. (4)(5) The patient’s clinical presentation and history, however, may lead the provider to attribute the signs and symptoms to other conditions such as a cerebrovascular accident, status epilepticus, intoxication, sepsis, traumatic injury or severe psychotic agitation. (6-10) rather than to hypoglycemia Patients with hypoglycemia may present to the ED with a range of signs and symptoms that can be divided into two broad categories: neuroglycopenic and hyperepinephrinemic. As glucose is the main energy source for the CNS, it is not surprising that most episodes of symptomatic hypoglycemia present with neurologic dysfunction. When there is a decline in serum sugar, the brain quickly exhausts its reserve supply of carbohydrate fuel, thus resulting in CNS dysfunction, which is manifested most commonly as alteration in consciousness such as lethargy, confusion, and unresponsiveness. More importantly, for the psychiatrist, the patients may present with agitation and combativeness. Other neuroglycopenic manifestations include convulsive activity and the development of focal neurologic deficits. A review of 125 cases of hypoglycemia presenting to an urban ED showed that the neuroglycopenic findings predominated. (4) Depressed sensorium was noted in 52% of cases, with other mental status changes (e.g., agitation and combativeness) found in 30% of patients. Described less frequently, seizure activity and focal neurological findings were encountered in 7% and 2% of of patients, respectively. (4) In the absence of neuronal damage, these neurologic deficits should reverse with the administration of glucose and do not require aggressive evaluation such as a computed tomography (CT) scan of the head.

Case Report:
Mr. X is a 56-year-old African American male with history of schizoaffective disorder and multiple prior psychiatric admissions, resident of a community residence who was brought in by police to the psychiatric emergency room secondary to agitation and combative behavior at his residence. Medical history was significant for diet-controlled hypertension; old Apical MI and GI bleed in 1992. In the ER Mr. X was calm and cooperative and claimed that other residents were bothering him at the community residence. Mr. X was admitted to the psychiatric ward and put on his usual medications which included:

Depakote 500 mg orally BID
Seroquel 200 mg orally BID
Haldol 5 mg orally BID
Trilafon 16mg orally in am and 32 mg orally at bedtime
Ativan 0.5 mg orally BID

Once on the psychiatric unit Mr. X immediately became extremely agitated. He was yelling, screaming, making animal sounds, banging his head against the wall and his speech was incoherent. His eyes were rolled back and he became very combative which prompted the physician on call to restrain the patient for his own safety. He was given cogentin 2mg IM secondary to his EPS like presentation as he was on high doses of multiple psychotropics however there was no change in his condition. While on restraints the patient had streaks of red dried blood coming out of his mouth. Because of severe agitation patient was given 6 mg of ativan in divided doses, which controlled his agitation for only a brief period of time before he became combative again. Stat neurological and medical consultations were sought. According to the neurologist a seizure was unlikely as patient was conscious and neurological exam was non-focal. Medical consult could not identify any obvious cause for this unusual presentation and decided to transfer the patient to medical intensive care unit for further management. The initial investigations revealed:

Vitals: T 98.8F, P 107,R 18, BP
Urine toxicology- negative
CMP- Blood glucose of 10mg/dL, Electrolytes WNL
CT scan head- Negative for any bleed

Mr. X was given 50% IV glucose and repeat blood sugar was done which was 22mg/dL. Patient’s condition started to improve and after two hours the blood glucose was 210mg/dL. By that time there was marked change in Mr. X’s condition and his only complaint was hunger. He was transferred to medical floor and psychiatric and endocrinology consult were sought. Psychiatric consult did not believe that sudden change in the blood glucose was due to any psychotropic medications. Endocrinology workup was negative for any obvious cause of hypoglycemia including insulinoma and extra pancreatic neoplasms. All three specialties agreed that patient’s low blood sugar could have been a result of exogenous insulin or oral hypoglycemic administration most likely due to medication error at the community residence. Mr. X was discharged to the community residence in stable condition.

Research in healthy adults shows that mental efficiency measurably declines as blood glucose falls below 65mg/dL. The actual level of blood glucose that causes CNS deprivation and produces symptoms is highly individual. The glucose level may be influenced by factors such as age, sex, weight, dietary history, physical activity, emotion, and coexisting disease. Many reports exist of asymptomatic individuals with plasma glucose levels of 35 mg/dL or lower and of individuals who are symptomatic with glucose levels in the normal range. The actual value of plasma glucose that defines hypoglycemia is somewhat arbitrary. The clinical state of the patient must be correlated with the glucose determination. Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (adrenaline and glucagon) triggered by the falling serum glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

Adrenergic Manifestations
• Shakiness, anxiety, nervousness, tremor
• Palpitations, tachycardia
• Sweating, feeling of warmth
• Pallor, coldness, clamminess
• Dilated pupils
Glucagon Manifestations
• Hunger, borborygmus
• Nausea, vomiting, abdominal discomfort
Neuroglycopenic Manifestations
• Abnormal mentation, impaired judgment
• Nonspecific dysphoria, anxiety, moodiness, depression, crying, fear of dying
• Negativism, irritability, belligerence, combativeness, rage
• Personality change, emotional lability
• Fatigue, weakness, apathy, lethargy, daydreaming, sleepiness
• Confusion, amnesia, dizziness, delirium
• Staring, "glassy" look, blurred vision, double vision
• Automatic behavior
• Difficulty speaking, slurred speech
• Ataxia, incoordination, sometimes mistaken for "drunkenness"
• Focal or general motor deficit, paralysis, hemiparesis
• Paresthesias, headache
• Stupor, coma, abnormal breathing
• Generalized or focal seizures

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms. Specific manifestations vary by age and by the severity. In young children, vomiting often accompanies morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects. The symptoms of a single person do tend to be similar from episode to episode.

Causes of Hypoglycemia
• Fed –reactive states
• Postprandial Insulin
• Alimentary Factitious
• Early diabetes mellitus
• Sulfonylureas
• Idiopathic Alcohol
• Fasting
• Miscellaneous drugs
• Islet-cell tumor of pancreas
• Posthyperalimentation
• Iinsulinoma
• Hemodialysis
• Extrapancreatic neoplasm’s
• Endocrine-related
• Pituitary insufficiency
• Adrenal insufficiency
• Glucagon deficiency
• Thyroid insufficiency
• Hepatic disease
• Miscellaneous
• Sepsis
• Chronic renal failure
• Starvation
• Autoimmune
• Exercise
• Artifactual
Potentially Hypoglycemic Agents
• Acetaminophen
• Amphetamine
• Aspirin
• Chloramphenicol
• Dextropropoxyphene
• Dicumarol
• Oxytetracycline
• Disopryamide
• Ethylenediaminetetraacetate
• Halofenate
• Haloperidol
• Hypoglycin (akee nut)
• Kerola (herb)
• Lithium
• Manganese
• Monoamine oxidase inhibitors
• Onion extract
• Orphenadrine
• Pentamidine
• Phenothiazines
• Phenylbutazone
• Propranolol
• Quinine
• Sulfa drugs

Plasma glucose levels should be determined in all patients who are comatose, have a seizure, have a disturbance of sensorium, have taken a drug overdose, smell of alcohol, or have funny spells that are undefined. Random glucose levels should be determined in all diabetic patients with clinically significant complaints who come to the psychiatric ED.

Hypoglycemia may present without classic symptoms especially in elderly patients and may imitate every neurological symptom. Our case illustrates the importance of considering hypoglycemia in every case of change in mental status, acute neurological deficits, acute psychosis, acute agitation even when clinical findings seem to be explained by other causes. An immediate blood glucose test should be done to exclude hypoglycemia.

1. Luber S, Brady W, Brand A, et al. Acute hypoglycemia masquerading as head trauma: A report of four cases. Am J Emerg Med 1996; 14:543-547.
2. Pollock G, Brady WJ, Hargarten S, et al. Hypoglycemia manifested by sinus bradycardia: A report of three cases. Acad Emerg Med 1996; 3:700-707.
3. Fink S, Chaudhuri TK. Iatrogenic hypoglycemia and malpractice claims. South Med J 1997; 90:251-253
4. Malouf R, Brust JCM. Hypoglycemia: Causes, neurological manifestations, and outcome. Ann Neurol 1985; 17:421-430.
5. Seltzer HS. Drug-induced hypoglycemia: A review based on 473 cases. Diabetes 1972; 21:955-966.
6. Wallis WE, Donaldson I, Scott RS, et al. Hypoglycemia masquerading as cerebrovascular disease (hypoglycemic hemiplegia). Ann Neurol 1985; 18:510-512.
7. Foster JW, Hart RG. Hypoglycemic hemiplegia: Two cases and a clinical review. Stroke 1987; 18:944-946.
8. Brady WJ, Duncan CW. Hypoglycemia masquerading as acute psychosis and acute cocaine intoxication. Am J Emerg Med 1999; 17:318-319.
9.Luber S, Meldon S, Brady W. Hypoglycemia presenting as acute respiratory failure in an infant. Am J Emerg Med 1998; 16:281-284.
10. Luber S, Brady W, Brand A, et al. Acute hypoglycemia masquerading as head trauma: A report of four cases. Am J Emerg Med 1996; 14:543-547.

First Published December 2005

Copyright Priory Lodge Education 2005

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