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Old 12-13-2012
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Arrow A 36-year-old woman with hyponatremia

A 36-year-old woman presents to the ED after experiencing a seizure in her apartment 3 hours earlier. She has no known prior medical problems, and takes only aspirin for some recent headaches. She is currently lethargic but responsive and coherent. Her temperature is 37.2°C (98.9°F), blood pressure is 117/68 mm Hg with no orthostatic changes, and pulse is 70/min. Physical examination reveals anicteric sclerae with reactive pupils and moist mucous membranes.
Laboratory tests show:
Na+ 124 mEq/L
Ca2+ 9.8 mg/dL
Cl− 100 mEq/L
HCO3 − 19 mEq/L
Blood urea nitrogen 9.2 mg/dL
Creatinine 0.9 mg/dL
Glucose 110 mg/dL
Liver function tests, amylase, lipase, and bilirubin are normal. Urine electrolytes reveal an elevated urine sodium. Which of the following is the most likely cause of this patient’s hyponatremia?

(A) Bartter’s syndrome
(B) Brain tumor
(C) Hyperglycemic crisis
(D) Primary biliary cirrhosis
(E) Subarachnoid hemorrhage
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(E) sub arachnoid hemorrhage

Hyponatremia is common after SAH , there are multiple etioligies with the most common being syndrome of inappropriate ADH secretion (SIADH)
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Quote:
Originally Posted by adeelacheema View Post
(E) sub arachnoid hemorrhage

Hyponatremia is common after SAH , there are multiple etioligies with the most common being syndrome of inappropriate ADH secretion (SIADH)
I agree with u but i believe if serum potassium is Shawn we would definitely be sure. because in bartter syndrome there is low k and metabolic alkalosis in the presence of normal BP.but i would definitely choose SAH in this condition
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ans B........
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Quote:
Originally Posted by Hitman View Post
ans B........
do u know what does bug me, that high urine Na it really goes with bartter but. i really dont know what do u think?
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Quote:
Originally Posted by the_emperor View Post
do u know what does bug me, that high urine Na it really goes with bartter but. i really dont know what do u think?
Bartter’s syndrome is a defect in sodium transport at the loop of Henle leading to hypokalemia, metabolic alkalosis, and hypercalciuria. It presents early in life and is associated with growth defects, low blood pressure, and mental retardation. It is not asso-ciated with hyponatremia.
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B brain tumour or lung tumor (small oat cell) correspond with siadh , another important concept is euvolemic status in this individual initial hypervolemia causes dec renin thus dec aldosterone and this salt wasting causing urine osmolarity to increase
Ams seizure typical of hyponattemia

Treated with demeocyxline to induce dinsipidus


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Quote:
Originally Posted by rahulmbbsmd View Post
B brain tumour or lung tumor (small oat cell) correspond with siadh , another important concept is euvolemic status in this individual initial hypervolemia causes dec renin thus dec aldosterone and this salt wasting causing urine osmolarity to increase
Ams seizure typical of hyponattemia

Treated with demeocyxline to induce dinsipidus


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then it should be SIADH due to brain tumor because the high urine Na is goes with that. and SAH is less likely cuz of absence typical feature.. in bartter the BP could also be normal
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I still think its SAH, due to her age history and sudden onset of symptoms, signs of cerebral edema ( seizures, confusion, coma) appear when hyponatremia is severe Na < 120 mOsm Or its ACUTE in onset .

SAH sounds the most probable with all this evidence , brain tumor would have a slow onset plus other symptoms , same goes for lung carcinoma ( cough , wt loss , dyspnea , age)
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Quote:
Originally Posted by adeelacheema View Post
I still think its SAH, due to her age history and sudden onset of symptoms, signs of cerebral edema ( seizures, confusion, coma) appear when hyponatremia is severe Na < 120 mOsm Or its ACUTE in onset .

SAH sounds the most probable with all this evidence , brain tumor would have a slow onset plus other symptoms , same goes for lung carcinoma ( cough , wt loss , dyspnea , age)
could be but do not forget that SAH is not a walk in the park giving LOC in 50% of cases and moreover there is no dramatic symptoms of severe headache, photo phobia. and u can not explain high urine Na. do not forget USMLE cases should be typical.
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Agree with above Isn't sah worst headache pp m9 like while tumour a diffuse headache which might be medicated with aspirin , sometimes wake u from sleep

Keep typical in mind , still if like
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Why u Ed doc no ct , lol

Ed doc is thinking metabolic 1st right
Neways good q, remember urine body sodium and euvolemic status

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Quote:
Originally Posted by heartbeat View Post
A 36-year-old woman presents to the ED after experiencing a seizure in her apartment 3 hours earlier. She has no known prior medical problems, and takes only aspirin for some recent headaches. She is currently lethargic but responsive and coherent. Her temperature is 37.2°C (98.9°F), blood pressure is 117/68 mm Hg with no orthostatic changes, and pulse is 70/min. Physical examination reveals anicteric sclerae with reactive pupils and moist mucous membranes.
Laboratory tests show:
Na+ 124 mEq/L
Ca2+ 9.8 mg/dL
Cl− 100 mEq/L
HCO3 − 19 mEq/L
Blood urea nitrogen 9.2 mg/dL
Creatinine 0.9 mg/dL
Glucose 110 mg/dL
Liver function tests, amylase, lipase, and bilirubin are normal. Urine electrolytes reveal an elevated urine sodium. Which of the following is the most likely cause of this patient’s hyponatremia?

(A) Bartter’s syndrome
(B) Brain tumor
(C) Hyperglycemic crisis
(D) Primary biliary cirrhosis
(E) Subarachnoid hemorrhage
I would go with B...what is the answer???
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Brain tumor
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The correct answer is B.
This patient has a normal blood pressure and heart rate, moist mucous membranes, and gives no history of recent fluid losses. She demonstrates euvolemic hyponatremia without symptoms of acute water intoxication such as confusion, anorexia, nausea, vomiting, or coma. Common causes of euvolemic hyponatremia include the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), a reset osmostat, and isotonic salt losses with free water repletion. In this case, the patient has experienced recent onset of headaches and now a seizure, raising the possibility of a slowly progressing intracranial process. A hyponatremic seizure at a sodium concentration of 124 mEq/L is unlikely given the clinical scenario of a chronic disorder. The history of recent-onset headaches and seizure should raise concern for intracranial malignancy, which is often associated with inappropriate ADH secretion from the pituitary gland. This is confirmed by elevated urine sodium levels in the setting of clinically normal volume status. Nonsteroidal anti-inflammatory drugs potentiate the action of ADH and are also associated with development of SIADH.

Other intracranial processes (subarachnoid hemorrhage) are associated with a process known as cerebral salt wasting, thought to be due to increased levels of brain natriuretic peptide and concurrent aldosterone suppression. Despite hyponatremia and high plasma antidiuretic hormone, cerebral salt wasting can be differentiated from the syndrome of inappropriate secretion of antidiuretic hormone by signs and symptoms of hypovolemia.
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