Case Vignettes in Neurology

PATIENT CASE STUDIES

Case 30
Case discussion A 75-year old diabetic, non hypertensive, male had a several week history of malaise, generalized weakness and confusion in association with poor control of his diabetes. He progressively became more stuporose over a three day period. He had a generalized seizure and was admitted to the hospital unconscious. On examination he was comatose, responsive to deep pain with eye opening and moaning. Vital signs were stable, BP 120/60, pulse 96, regular, respiratory rate 18. Temperature was 37.5 C. Pupils were sluggishly reactive to light. Oculocephalic reflexes were present. A right facial droop was present. There was a moderate right hemiparesis with 4/5 power right upper and lower extremities.. DTRs were 1 and symmetric in the upper extremities and absent in the lower extremities. Both plantar reflexes were extensor. Urinalysis revealed glycosuria, moderate bacteria and white cells and no ketones.
Summarize the Case in 1-2 sentences. This patient is a 75 year old male Diabetic who presented with several weeks of weakness and confusion which progressed into a seizure and loss of consciousness over three days. Exam shows sluggish pupil response, a rt sided hemiparesis and facial droop, decreased DTRs, and a positive Babinski. Do you think the several week course was a progressive one? in summary you could say there were both UMN with a right hemiparesis and extensor plantar reflex and lower motor neuron signs with absent dtrs. (decreased in the arms, absent in the legs) Discuss lesion localization on the basis of the physical examination. CNS (confusion, seizure, loss of consciousness, hemiparesis, Babinski sign); brainstem- Rt CN 7 (facial droop); peripheral neuropathy (decreased DTRs). Coma: brain stem or diffuse cortical where is the lesion causing seziure where is the lesion causing hemiparesis? where are the lesions causing bilateral Babinski’s. why is facial droop a right cn 7 lesion? peripheral neuropathy is good Discuss underlying pathogenesis on the basis of clinical course. Worsening course over 3 days (subacute) suggesting infectious pathogenesis or tumor or sub-acute complication of Diabetes. Patient also has chronic underlying neuropathy suggesting metabolic pathogenesis. Second sentence is irrelevant to the question. the question is not asking you to make a dx (eg complication of diabetes); rather you could have said that subacute course could be a metabolic process. Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses. Diabetic neuropathy with hyperosmolar coma. Alternatively: tumor, sepsis The hyperosmolar coma is clearly the most important here (why mention the neuropathy first) Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis. Chem 20 (increased glucose, BUN, creatinine). Urine output (low) You need to check for a precipitating cause of the hyperosmolar coma, often this is an infection e.g. UTI. Indicate complications of the disease and ancillary tests that would help evaluate them. hyperosmolar coma is 50% fatal. Most likely close clinical observation is necessary to monitor patient's progress as therapy is given. If the patient survives, he or she may experience complications of systemic infections, strokes, systemic DIC, thrombosis, seizures, transient hemiplegia, acute pancreatitis. good Discuss how the underlying pathophysiology is relevant in the management of this patient. Because the patient is severely dehydrated (severe osmotic diuresis), IV fluids are administered in an attempt to rehydrate. Potassium may be required early on in treatment due to a shift intracellularly of potassium. The cause of neuropathy in diabetes is due to the excessive glycosylated proteins in the endothelium of vessels, resulting in disruption of the blood-nerve barrier with endonurial edema. The management for diabetic neuropathy is an aggressive control of serum glucose level. You do not address whether hyperglycemia is toxic to neurons and how.

Case 30

Case discussion

A 75-year old diabetic, non hypertensive, male had a several week history of malaise, generalized weakness and confusion in association with poor control of his diabetes. He progressively became more stuporose over a three day period. He had a generalized seizure and was admitted to the hospital unconscious.

On examination he was comatose, responsive to deep pain with eye opening and moaning. Vital signs were stable, BP 120/60, pulse 96, regular, respiratory rate 18. Temperature was 37.5 C. Pupils were sluggishly reactive to light. Oculocephalic reflexes were present. A right facial droop was present. There was a moderate right hemiparesis with 4/5 power right upper and lower extremities.. DTRs were 1 and symmetric in the upper extremities and absent in the lower extremities. Both plantar reflexes were extensor. Urinalysis revealed glycosuria, moderate bacteria and white cells and no ketones.

Summarize the Case in 1-2 sentences.

This patient is a 75 year old male Diabetic who presented with several weeks of weakness and confusion which progressed into a seizure and loss of consciousness over three days. Exam shows sluggish pupil response, a rt sided hemiparesis and facial droop, decreased DTRs, and a positive Babinski.

Do you think the several week course was a progressive one? in summary you could say there were both UMN with a right hemiparesis and extensor plantar reflex and lower motor neuron signs with absent dtrs. (decreased in the arms, absent in the legs)

Discuss lesion localization on the basis of the physical examination.

CNS (confusion, seizure, loss of consciousness, hemiparesis, Babinski sign); brainstem- Rt CN 7 (facial droop); peripheral neuropathy (decreased DTRs).

Coma: brain stem or diffuse cortical where is the lesion causing seziure where is the lesion causing hemiparesis? where are the lesions causing bilateral Babinski’s. why is facial droop a right cn 7 lesion? peripheral neuropathy is good

Discuss underlying pathogenesis on the basis of clinical course.

Worsening course over 3 days (subacute) suggesting infectious pathogenesis or tumor or sub-acute complication of Diabetes. Patient also has chronic underlying neuropathy suggesting metabolic pathogenesis.

Second sentence is irrelevant to the question. the question is not asking you to make a dx (eg complication of diabetes); rather you could have said that subacute course could be a metabolic process.

Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses.

Diabetic neuropathy with hyperosmolar coma.

Alternatively: tumor, sepsis

The hyperosmolar coma is clearly the most important here (why mention the neuropathy first)

Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis.

Chem 20 (increased glucose, BUN, creatinine).
Urine output (low)

You need to check for a precipitating cause of the hyperosmolar coma, often this is an infection e.g. UTI.

Indicate complications of the disease and ancillary tests that would help evaluate them.

hyperosmolar coma is 50% fatal. Most likely close

clinical observation is necessary to monitor patient's progress as therapy is given.

If the patient survives, he or she may experience complications of systemic infections, strokes, systemic DIC, thrombosis, seizures, transient hemiplegia, acute pancreatitis.

good

Discuss how the underlying pathophysiology is relevant in the management of this patient.

Because the patient is severely dehydrated (severe osmotic diuresis), IV fluids are administered in an attempt to rehydrate. Potassium may be required early on in treatment due to a shift intracellularly of potassium. The cause of neuropathy in diabetes is due to the excessive glycosylated proteins in the endothelium of vessels, resulting in disruption of the blood-nerve barrier with endonurial edema. The management for diabetic neuropathy is an aggressive control of serum glucose level.

You do not address whether hyperglycemia is toxic to neurons and how.