Sequelae following hypoglycemic coma are rare, dependent on the severity and duration of hypoglycemia, and include profound memory loss, persistent vegetative state, and death in 2 to 4% of cases. MRI reports are limited and characterized by lesions that involve cerebral cortex, hippocampus, and basal ganglia.1-3⇓⇓ Diffusion-weighted MRI (DWI) detects change in water diffusion with cellular dysfunction and primarily identifies early ischemic changes in stroke.4 We here report DWI in association with hypoglycemic coma and consider its prognostic importance.
Case history.
A 53-year-old man with insulin-dependent diabetes mellitus and HIV infection was taken to the Hartford Hospital emergency department after being found unresponsive at home. A friend found the patient “sleeping” and gave him his morning insulin dose; when he failed to awaken after several hours, emergency medical services was called. On arrival they found the patient unresponsive with pinpoint pupils, shallow respirations, and hypotension. Blood glucose was 23 mg/dL and the patient was given 1 mg of glucagon and 1.4 mg of naloxone hydrochloride IM without improvement. Medical history included alcohol abuse and prior IV drug use, currently treated with methadone, and previous episodes of loss of consciousness with hypoglycemia. In the emergency department he was noted to be in respiratory distress, was intubated, and was given 50 mL of 50% dextrose IV.
Physical examination.
The patient had a temperature of 101 °F, with otherwise stable vital signs. He opened his eyes to painful stimulation, demonstrated no evidence of comprehension, had spontaneous respirations, and showed no other motor activity. Doll’s eyes were intact, pupils were 2 mm and nonreactive. The deep tendon reflexes were absent and the plantar response was flexor with the remainder of the neurologic examination showing no focal abnormality.
Laboratory studies.
Complete blood count other than moderate anemia was normal. Electrolytes, blood urea nitrogen, creatinine, blood glucose, and blood gases were all within the normal range. A routine urinalysis and urine toxicology screen was negative. CSF, glucose, protein, cell count, culture and smear, and India ink preparation were normal or negative. CD4 count was 70.
A CT scan of the head on admission was unremarkable and a repeat CT scan after 4 days showed subtle decreased attenuation of the basal ganglia ( figure, H). Neuroimaging on day 5 showed hyperintense signal of the basal ganglia, hippocampus, and cerebral cortex bilaterally on DWI (figure, A through C), more so than on the fluid-attenuated inversion recovery (figure, D through F) and T2-weighted sequences, with hypointense signal in the basal ganglia on MRI apparent diffusion coefficient map (figure, G). Basal ganglia on T1-weighted sequences were unremarkable apart from the slight enhancement with gadolinium. The EEG showed bilateral diffuse slowing of the delta range.
Figure. Transverse diffusion-weighted imaging (b = 1000 s/mm2; effective gradient, 23 mT/m; repetition time msec/echo time msec, 9999/93; matrix, 128 × 128; field of view, 360 × 220 mm; section thickness, 6 mm with 0-mm gap) with bilateral hyperintense signal of hippocampus (A), cortex of the temporal lobe (B), and caudate and lenticular nucleus (C) is shown. Transverse fluid-attenuated inversion recovery (9002/148/1 inversion time = 2200) images (D, E, F) corresponding to diffusion-weighted MR images are also shown. Transverse apparent diffusion coefficient map displays hypointense signal of the basal ganglia (G). CT scan shows subtle decreased attenuation of the striatum (H).
Over the next 5 days the patient’s neurologic condition failed to improve. Considering the underlying HIV infection, the diffuse abnormality on neuroimaging, and overall poor prognosis, the family decided to withdraw life support measures. He was transferred to the palliative care unit where he died on the eighth hospital day.
Discussion.
MRI in hypoglycemic coma variably involves the cortex, hippocampus, and basal ganglia.1-3⇓⇓ The most severely affected patients manifest bilateral basal ganglia signal abnormality, which correlates with the neuropathologic change in patients with fatal hypoglycemia.5 The five reported cases with basal ganglia involvement2,3⇓ survived in a persistent vegetative state, whereas those with the basal ganglia spared1 survived with lesser degrees of neurologic impairment.
Distinct from MRI, DWI serves as a chronologic marker with abnormal signal that may appear within minutes of brain insult and resolve over several weeks. DWI abnormalities seen in our case better define the areas of involvement and at an earlier time than conventional MRI. Changes of the basal ganglia with DWI in association with hypoglycemia have previously been described in animal studies but only when combined with hypoxia,6 implying associated hypoxic damage in patients with basal ganglia involvement. The MRI and DWI lesions seen in our patient correspond with the MRI location (basal ganglia,2,3⇓ hippocampus,1-3⇓⇓ and temporal lobe cortex1) and signal abnormality (hyperintense T2-weighted sequences)1,3⇓ previously reported. The difference in signal intensity described by others2 may be due to paramagnetic changes due to diapedesis of red cells through damaged capillary endothelium, related to a delay in imaging following hypoglycemia (range 8 to 246 days) and associated hypoxic ischemic encephalopathy.7 Changes of the basal ganglia in hypoglycemic coma portend a poor outcome and as such the DWI findings described here may prove helpful particularly in timely decisions regarding life support measures.
- Received March 19, 2001.
- Accepted May 12, 2001.
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