5/11/2020- Monday

Diabetic ketoacidosisà consequence of insulin deficiency & counter regulatory hormone excess. Its usually a complication of Diabetes type 1 and is an acute, life-threatening condition. If left untreated it will result in worsening hyperglycemia, ketone formation from cellular starvation and a wide anion gap metabolic acidosis. This metabolic acidosis is due when free fatty acids are transported to liver and undergo conversion to ketone bodies.

Causes:

DKA usually is a response to stressful triggers such as infection (which is the most common cause of DKA) UTI or pneumonia.

Discontinuation or inadequate insulin therapy, undiagnosed diabetes or pancreatitis can also cause DKA.

Signs/Symptoms:

Tachycardia

Hypotension

Dry mucous membranes

Decreased skin turgor

Fruity odor on breath

Altered mental status

Kussmaul respirations (deep, labored breathing pattern that indicates that the body or organs have become too acidic. The body is constantly doing work to maintain an average temperature and neutral blood acidity)

Polyuria/Polydipsia.

Abdominal pain.

Diagnosis:

POC Glucose, EKG, CBC, CMP, Lipase, Blood gas, phosphate, magnesium Urinalysis

Glucose > 250 mg/dL

OR Anion gap > 10mEq/L

OR Bicarbonate < 15 mEq/L (metabolic acidosis).

OR pH <7.3 (acidotic state)

With ketonuria(urine) or ketonemia(blood) constitute the diagnosis of DKA

Significant electrolyte deficiency (derangements) secondary to osmotic diuresis

Hyponatremia/ Hypokalemia

Hypomagnesemia/ Hypophosphatemia

Management:

Management: Fluids, Cardiac, pulse oximetry

2 Large Bore IVs, NS bolus 2-4L bolus or 20ml/kg/hour for first hour

If pH is ≤ 6.9 à we can start giving sodium bicarbonate until that pH goes to 7. Only use sodium bicarbonate if that pH is less than 6.9.

Next, we can start with insulin. Before we give insulin to these patients, we have to check their potassium levels. The reason why we check their potassium is because insulin will shift K+ back into cells and out of serum, decreasing the levels of potassium. If our patient has low levels of potassium, insulin should not be administered until potassium is back to normal levels.

Insulin gtt (drip) – 0.1 units/kg/hr (know this)

If K+ is >5.2 can initiate  gtt repeat K+ q2h

If K+ is 3.3 – 5.2, add K+ to each liter of fluid given and initiate drip with repeat K+ q2h

If K+ < 3.3, hold insulin gtt and replete K+ until >3.3

Once serum glucose is 200 mg/dL add dextrose to IV fluids and reduce gtt to 0.05

Until you meet other goals of treatment.

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Wednesday- 5/13/2020

Abdominal aortic aneurysm:

Risk factors: advance age (over 60 years old), smoking, Caucasian, males, arthrosclerosis, connective tissue disorder such as Marfan disorder.

Pathophysiology:

Abdominal aortic aneurysms tend to occur when there is a failure of the structural proteins of the aorta which can result in gradual weakening of the aortic wall. Most abdominal aortic aneurysm occur in the infrarenal site and that’s due to lower units of structural proteins in that area.

Signs/Symptoms:

Most patients will present as asymptomatic. Some are found incidentally on imaging while screening for another condition. Some are found during physical exams as a palpable abdominal mass or abdominal bruit.

In patients who are symptomatic and unruptured aneurysm, they often present with abdominal flank pain or back pain. They will also have pulsating abdominal mass which is non-tender and abdominal bruit.

In patients who are symptomatic and have a ruptured aneurysm, they will have all the symptoms mentioned above and in addition they will also be hypotensive and have syncope as well. Patients with ruptured aneurysm can also present with diffuse abdominal pain, distention, and flank ecchymosis (Cullen (umbilical) or Grey-Turner Sign (flanks). Most of these patients will die before making into the emergency room.

Diagnosis:

Screening: one-time screening via abdominal ultrasound in men 65-75 years old who have ever smoked.

In those patients who are hemodynamically stable and asymptomatic, abdominal ultrasound is the initial test and we can also use ultrasound to monitor progression of aneurysm if not rupture.

In those patients who are hemodynamically stable but symptomatic, is a CT scan with IV contrast. CT scan can help determine the exact location, size, and involvement of other vessels. For those patients with allergies to contrast, MRA (Magnetic Resonance Angiogram) is an option

In those patients who are hemodynamically unstable and symptomatic, a focused bedside ultrasound is the initial study as your suspicion for a AAA is high and immediate management is indicated.

Labs: CBC, CMP, PT/PTT (bleeding), T/S (type and screen), blood gas w/ lactic acid, troponin

Management:

Stable: have large bore IV ready.

Vascular consult

Use beta- blockers to decrease expansion and rupture risk.

Ruptured: Immediate surgical repair (Open surgical repair via transabdominal approach has been the gold standard).

2 large bore IV’s

Transfusion  + fluid resuscitation

If patient on Plavix/ASA à give platelets

If patient on warfarin à FFP & Vitamin K or Kaysentra

Treatment is also based on the size and rate of expansion of the aneurysm. If the aneurysm is more than 5.5 cm or expanding more than 0.5 cm in 6 monthsà immediate surgical repair even if asymptomatic.

Less than 4.5à vascular surgeon referral

3-4.5 cmà monitor with ultrasound every 6 months.

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Friday- 5/15/2020

Torsades de pointes:

Torsades is 2 to 3 more common in women than in men. Women will present with longer QT intervals as well as have more QT prolongation secondary to drug therapy then men. The highest frequency of torsades is in patients ages 35 to 50 years old.

Torsades de pointes is considered a variant of ventricular tachycardia. Its part of polymorphic ventricular tachycardia where we see waxing and waning QRS amplitude on the EKG. In torsades, the QRS complexes vary from beat to beat and the ventricular rate can range from 150 beats to 250 bpm. Torsades de pointes means “twisting of the point” as it will look exactly like that on an EKG. If there is prolonged repolarization and early after-depolarization we can see the formation of torsades de pointes.

Causes:

There are a few causes that lead to torsades de pointes: Prolonged QT interval is a pretty common cause of torsades.

Electrolyte abnormalities such as hypomagnesemia, hypokalemia, hypocalcemia can also precipitate torsades.

Different medications can also lead to torsades. Digoxin, class IA antiarrhythmic such as quinidine, procainamide and disopyramide can precipitate torsades. Other medications such as class III antiarrhythmics such as sotalol and ibutilide can also lead to torsades. Lastly antibiotics such as macrolides are also associated with torsades.

Signs/Symptoms:

Patients with torsades will present with recurrent episodes of palpitations, dizziness and syncope.

In young patients with torsades, we should also use their family history to see if there is any one from their family with recent sudden cardiac death or sudden infant death syndrome. In young patients, episodes of torsades are triggered by adrenergic stimulation such as stress, fear, or physical exertion.

Diagnosis:

EKG will show polymorphic ventricular tachycardia and a prolonged QT interval and pathological U waves are also present. Patients can also have a short-long-short sequence between R-R intervals before trigger response.

We can also order labs to exclude hypomagnesemia and hypokalemia.

We can also order cardiac enzymes to rule out possible myocardial ischemia, especially in those with QT prolongation.

Management

Treatment of choice is IV magnesium sulfate. It suppresses early afterdepolarizations, terminating any potential arrythmias. Magnesium is effective in both terminating and preventing recurrent torsades. While administering magnesium we should also correct any underlying electrolytes abnormalities and also discontinue all drugs that are known to cause QT prolongation.

In refractory cases where the use of magnesium is not sufficient to treat torsades, we can also use isoproterenol and transvenous overdrive pacing.

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