History taking and careful observation (not laboratory results) were the authority upon which differential diagnoses and initial treatment plans were built. Laboratory tests confirmed (or not) our hypotheses, not the other way around.
- Osler and the Way We Were Taught
- Osler and the Way We Were Taught
Cerebral salt-wasting (sometimes called renal salt-wasting)
The most common presenting story for cerebral salt wasting is hyponatremia after aneurysmal subarachnoid hemorrhage. A few days after the hemorrhage the patient’s serum sodium begins to drop while the urine sodium increases. The patient’s fluid status also decreases, and the patient becomes hyponatremic and hypovolemic.
It is important to distinguish between cerebral salt wasting and SIADH as the two are treated with opposite treatment strategies. For cerebral salt wasting the patient is given fluids and sodium supplementation. For SIADH the patient is fluid restricted.
Brain natriuretic peptide (BNP) is a bitch, and no one can change my mind about it
Hyponatremia + hypovolemia = Cerebral salt-wasting (CSW).
Hyponatremia + euvolemia or hypervolemia = SIADH.
Hyponatremia + euvolemia or hypervolemia = SIADH.
The key to understanding the pathophysiology, signs, symptoms, and treatment of SIADH is the awareness that the hyponatremia in this syndrome is a result of an excess of water and not a deficiency of Na+.
Today I’ve seen a case of receptive (Wernicke) aphasia in the hospital.
Lab Rats In Lab Coats
Today I’ve seen a case of receptive (Wernicke) aphasia in the hospital.
Patients with this type of aphasia usually have profound language comprehension deficits, even for single words or simple sentences. This is because in Wernicke’s aphasia individuals have damage in brain areas that are important for processing the meaning of words and spoken language. Such damage includes left posterior temporal regions of the brain, which are part of what is knows as Wernicke’s area.
The doctor asked him: where do you live?
He answered: I have this cough since a while.
He answered: I have this cough since a while.
DKA is no joke, it’s a serious condition that can lead to diabetic coma or even death. DKA is caused by an overload of ketones present in the blood.
When cells don't get the glucose they need for energy, the body begins to burn fat for energy, which produces ketones.
Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose -body’s normal source of energy-. When ketones build up in the blood, they make it more acidic.
When levels get too high, the patient can develop DKA.
DKA may happen to anyone with diabetes, though it is rare in people with type 2.
When cells don't get the glucose they need for energy, the body begins to burn fat for energy, which produces ketones.
Ketones are chemicals that the body creates when it breaks down fat to use for energy. The body does this when it doesn’t have enough insulin to use glucose -body’s normal source of energy-. When ketones build up in the blood, they make it more acidic.
When levels get too high, the patient can develop DKA.
DKA may happen to anyone with diabetes, though it is rare in people with type 2.
Patient presented with symptoms of diabetes which are: thirst, polyuria, weight loss and fatigue with symptoms of ketoacidosis which are epigastric pain, n&v.
On examination you’ll notice kussmaul breathing pattern, low SBP, tachycardia, cold extremities ”due to dehydration.”
On examination you’ll notice kussmaul breathing pattern, low SBP, tachycardia, cold extremities ”due to dehydration.”
The most common infections may precipitate DKA are: UTI and pneumonia. So on investigations we have to send for CXR and GUE. Ofc in addition to initial tests which are RBS for hyperglycemia, ABG for acidosis, CBC for elevated WBCs, serum potassium, And you can do ECG which may show signs of acute MI.
There are some criteria for admission to CCU:
Altered mental status, sock “ SBP less than 90”, patient’s age less than 5 yrs, pregnancy, Spo2 less than 92,bicarbonate less than 10, Potassium level less than 3,5 and Ph less than 7.
Altered mental status, sock “ SBP less than 90”, patient’s age less than 5 yrs, pregnancy, Spo2 less than 92,bicarbonate less than 10, Potassium level less than 3,5 and Ph less than 7.
Lab Rats In Lab Coats
There are some criteria for admission to CCU: Altered mental status, sock “ SBP less than 90”, patient’s age less than 5 yrs, pregnancy, Spo2 less than 92,bicarbonate less than 10, Potassium level less than 3,5 and Ph less than 7.
That’s why when we treat them, we never stop insulin unless the Ph becomes more than 7,3 and the bicarbonate more or equal to 15 mEq/l
,blood glucose less than 200 mg/dl and the patient is able to eat.
,blood glucose less than 200 mg/dl and the patient is able to eat.
In treatment don’t give insulin in the first hr, that may increase risk of cerebral edema and hypokalemia. Start with IV fluid only, then in the 2nd hour check the level of potassium before giving insulin because it may precipitate hypokalemia.
Few days ago I’ve seen a patient with epigastric pain and elevated level of amylase and WBCs. I thought it’s pancreatitis🥲 while it was DKA depending on other signs and symptoms.
And yes amylase level will be high in patients with DKA.
And yes amylase level will be high in patients with DKA.