A Kamha
Consultant Intensivist Physician. Head of Medical Intensive Care Unit. Hamad Medical Corporation. Doha, Qatar Tel:+974/4391619 akamha@hmc.org.qa
SMJ 2008 53(4): 10
Abstract
We report a patient with epilepsia partialis continua (EPC) associated with non ketotic hyperosmolar hyperglycemia. EPC is uncommon presenting clinical finding during nonketotic hyperglycemia. This case was reported in Medical Intensive Care Unit (MICU) in Hamad Medical Corporation, Doha, Qatar.
Keywords: Epilepsia partialis continua, hyperglycemia
Introduction:
The association between non-ketotic hyperglycemia (NKG) and epilepsia partialis continua (EPC) is rare but well known. We report a patient who presented with NKG and EPC who was admitted to the Medical Intensive Care Unit (MICU) in Hamad Medical Corporation in Qatar. It is vital to recognize the association between those conditions as correcting the metabolic abnormalities is the main step to treat the seizures.(1)
Case report
A 52 years old Pakistani right handed woman presented to Emergency Department with polyuria and polydipsia for four days. Also she had recurrent abnormal movements in the left hand with progressive involvement of the upper limb that started abruptly three days earlier. There was no significant past medical history. She was not talking any medication. In Emergency Department the blood sugar was found to be more than 24 mmol/l when tested by glucometer. The vital signs, heart, lung and abdominal examination were normal apart from sinus tachycardia. However, her head was intermittently turning to the left side with abduction and external rotation of the left arm. Glasgow Coma Scale was 10/15.
Laboratory results showed that blood sugar of 96 mmol/L (1728 mg), serum sodium of 123 meq/L, potassium level of 5.6 meq/L and serum osmolarity of 375 mOsm/L. There were negative ketons in blood and urine with bicarbonate level of 24 mmol/L. Blood gases showed normal Ph 7.39. Lumbar puncture showed normal cells, normal protein and only increased Cerebrospinal fluid glucose level (22 mmol/L). CT (Computerized tomography) and MRI (Magnetic resonance imaging) head were done and both were normal. EEG
(Electroencephalogram) (fig 1) showed frequent epileptiform discharges involving the frontocentral area which consistence with EPC. Carbamazepine 400 mg daily was started. Correction of metabolic disorder (Nonketotic hyperglycemia) with proper fluid replacement and insulin intravenous drip resulted in a gradual reduction in the number of seizures until they stopped over three days. Patient was stabilized and transferred to medical floor. She was seen by diabetic educator and discharged home in good condition. Carbamazepine was discontinued one month after discharge. No seizures were reported during nine months follow up.
EEG in EPC. · Generalized slowing of background activity with low amplitude sharp waves and spikes most prominent in frontoparietal area.
Discussion:
Seizures may result from any metabolic disorders but not commonly associated with nonketotic hyperglycemia. (1, 3) The pathogenesis of seizures from metabolic disorders is not completely understood. Hyperglycemia may precipitate EPC by reducing gamma-aminobutyric acid levels leading to a lower seizure threshold. (3, 4) On the other hand seizures are not usual associated with diabetic ketoacidos as ketosis and intracellular acidosis probably increase the seizure threshold. (1) In DKA, metabolic acidosis is often the major finding while serum glucose level is generally below 44 mmol/l. (5) In hyperosmolar hyperglycemic state there is little or no ketoacid accumulation, the serum glucose level usually exceeds 56 mmol/l, the serum osmolality may be increased up to 380 mosmol/kg, and neurologic abnormalities are frequently present. (5, 6, 7) Hyperglycemia may also precipitate EPC if there is asymptomatic structural cerebral lesion. (1) However, this is not the case in our patient as both CT and MRI head were normal.
EPC is defined as clonic muscular twitching repeated at fairly short intervals in one part of the body for a period of minutes, hours, days or weeks. (8) It is a form of focal status epilepticus manifesting as a continuous focal motor seizures.(9) It is usually associated with a wide range of EEG abnormalities including focal spikes and focal slow waves.(9) EEG was reported to be normal in some cases of EPC.(10)
Many conditions have been reported as a cause of EPC include structural abnormalities such as central nervous system tumors, trauma, cerebral infarction, intracerebral hemorrhage, cerebral abscess, and vascular malformation.(9) However in up to 50% of cases conventional brain imaging may be normal.(10) Metabolic abnormalities especially hyperglycemia, hyponatremia, and hepatic encephalopathy are a well known causes of EPC.(1) In the majority of cases with EPC precipitated by hyperglycemia occur before impairment of consciousness, therefore it is important to recognize this association.(8) Nonketotic hyperglycemia may be associated with many neurological signs such as focal seizures, EPC, myoclonus, impaired motor tone and impaired consciousness. (11, 12) This could lead to the diagnosis of previously undiagnosed diabetes mellitus and early reversal of the neurological condition. Focal seizures are usually resistant to antiepileptic drugs but usually respond to insulin and restoration of intravascular volume. (13, 14) These patients do not require long-term antiepileptic drug prophylaxis. (15)
Our patient was treated with insulin, intravenous fluids and a carbamazepine 400 mg daily. Her seizures resolved quickly and she has not had a recurrence. Treatment protocol for nonketotic hyperglycemia is the most important item in this situation. Treatment should include insulin therapy and correction of the fluid and electrolyte abnormalities that may be present. Special attention should be focused on airway, breathing and circulation (ABC). Initial fluid therapy is directed for restoration of intravascular volume and restoration of renal perfusion. The average fluid loss in nonketotic hyperglycemia is up to 8 to 10 liters. Fluid replacement should correct estimated deficits within 24 – 48 hours to avoid rapid reduction in the serum osmolality.(16) Regular insulin by continuous intravenous infusion is the treatment of choice. The target is usually to decrease serum glucose level by 2.5 to 4 mmol/L per hour. (17, 18) We consider that nonketotic hyperglycemia state is controlled when the patients are mentally alert and the plasma osmolality is below 320 mosmol/kg.
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