Category Archives: Morning Report
Aortic stenosis – 12/4/17
Most common etiologies of AS
- Calcification of a normal aortic valve overtime with age
- Bicuspid aortic valve
- Rheumatic heart disease (usually associated with mitral valve disease)
Symptoms
- Dyspnea (most common)
- Angina
- Syncope
Diagnosis
- Physical exam
- Systolic ejection murmur at RUSB with radiation to the carotids
- Any maneuver that decreases blood flow across the valve will cause a decrease in the sound of murmur (e.g. valsalva, handrip, or standing) whereas anything that increases blood flow across the valve will increase the sound of the murmur (e.g. squatting)
- Transthoracic echo
- Severe AS is AVA < 1 cm2, mean gradient greater or equal to 40, or max velocity greater than 4 m/s
Low-flow, low-gradient AS
- If patient has an AVA < 1 cm2 but has a mean gradient < 35 mmHg, consider low-flow, low-gradient AS
- To determine whether there is an intrinsic problem with the valve versus a pseduo-aortic stenosis due to myocardial dysfunction, do a dobutamine stress echo
- If AVA remains unchanged and the mean gradient increases with dobutamine, the etiology is severe AS and the patient would benefit from valve replacement
- If the AVA increases and the mean gradient doesn’t increase, this is a pseudo-aortic stenosis and the patient can be managed medically
When to treat?
- Any patient who is symptomatic
- An asymptomatic patient with EF < 50 or who is getting another cardiac surgery
Treatment
- AVR > TAVR if the patient is a surgical candidate
- TAVR is good for high risk patients and has similar survival to AVR in high-risk patients
- AV balloon valvuloplasty is a short-term bridge to TAVR as it only lasts a few months
- Medical management is usually not beneficial if a patient has severe AS
Giant Cell Arteritis – 11/28/2017
Aspirin toxicity – 11/22/17
Mechanism of action:
- Prostaglandins, prostacyclins, and thomboxane cause direct gastric mucosal injury
- Stimulation of chemoreceptor trigger zone in the medulla causes nausea/vomiting
- Activation of the respiratory center in the medulla causes hyperventilation and respiratory alkalosis
- Interference with cellular metabolism (Krebs cycle and oxidative phosphorylation) causes metabolic acidosis
Clinical features
- Tinnitus
- Vertigo
- Nausea and vomiting
- Diarrhea
- Hyperpnea (tachypnea and hyperventilation)
- Hyperthermia (due to disturbances with oxidative phosphorylation)
- Lethargy and confusion
Diagnostic tests
- Serum ASA level < 30 = therapeutic; > 40 = toxic; > 100 = absolute indication for HD regardless of symptoms
- Check K (goal is to prevent both hypo AND hyperkalemia), Cr (renal failure may indicate a need for HD), lactate (can increase due to direct cell injury), and PT (ASA can cause coagulopathy)
Treatment goals
- Keep salicyclate (which is a weak acid) in it’s charged and deprotonated form to prevent it from crossing into the blood brain barrier by maintaining alkalemia
Management
- ABCs – only intubate if evidence of HYPOventilation
- Activated charcoal if patient awake and oriented
- Sodium bicarbonate to keep urine pH ~ 8 and serum pH alkalotic and pH < 7.6 (still give bicarb even if evidence of alkalosis as long as pH < 7.6)
- IVF
- Prevent hypokalemia and HYPERkalemia because hyperkalemia can cause increase H secretion into the blood through the kidney H/K transporter which causes acidosis
- Glucose if altered mental status as neurohypoglycemia can be caused by ASA overdose despite a normal serum glucose level
- No acetazolamide because while that increases urine pH it causes increased H to be secreted into the blood causing acidosis which promotes the uncharged form of ASA which is toxic
Neurosyphilis – 11/21/2017
Panhypopituitaryism and adrenal crisis – 11/20/17
Remember that prolactin is inhibited by dopamine!
In panhypopituitaryism, the anterior pituitary hormones are more commonly affected than the posterior pituitary hormones and there is a spectrum for how much of the HPA axis is still preserved depending on the etiology of the panhypopituitaryism.
The hormones that need replacement in adults are T4 and cortisol. Testosterone can be replaced if needed in men. Estrogen and progesterone can be replaced in pre-menopausal women who do not want fertility at that time or in post-menopausal women to relieve post-menopausal symptoms. If a woman desires fertility and has enough HPA axis preserved then patients can get pulsatile GnRH to stimulate FSH and LH production to induce ovulation.
To screen for adrenal insufficiency, check a morning cortisol at 8am.
- Cortisol < 3 = likelihood high – check ACTH to determine primary versus secondary adrenal insufficiency
- Cortisol 3-18 = indeterminate – do further stimulation testing
- Cortisol > 18 = likelihood low – pursue other diagnosis
Stimulation tests
- Cosyntropin test – give cosyntropin (synthetic ACTH) and then measure cortisol level 1 hour later – normal is cortisol level > 18; if less than that, then likely primary adrenal insufficiency
- Insulin induced hyperglycemia test – give 0.1U/kg of insulin and check glucose at 15, 30, 60, 90, 120 minutes. Once glucose reaches < 50 then cortisol should be > 18
- Metyrapone testing – blocks 11B hydroxylase which leads to a drop in cortisol and increase in ACTH and increase in 11-deoxycortisol
Adrenal crisis
- Etiologies
- Insufficient dosing of steroids
- Failure to increase dosage of steroids with acute illness
- Persistent vomiting or diarrhea causing malabsorption of steroids
- Can commonly see isolated ACTH presentation in panhypopituitaryism
- Treatment
- Dexamethasone if adrenal insufficiency not yet diagnosed because it does not interfere with cortisol testing
- Hydrocortisone if pre-existing diagnosis
Remember – if you suspect adrenal insufficiency, give stress dose steroids immediately without waiting for further testing!
Cholangiocarcinoma – 11/15/2017
Pulmonary Hypertension – 11/14/15
Definition: mPAP greater or equal to 25 mmHg at rest
- Can also classify as pre and post-capillary
- Pre-capillary is group 1, 3, 4, 5
- Post-capillary is group 2 and 5
- Combination can be group 2 and 5
- If enough volume overload to cause enough right heart strain to cause intrinsic remodeling then group 2 could cause intrinsic PAH
- Best prognosis is CTEPH if able to surgically remove the clot (usually able to do so in proximal clots)
- Worst prognosis is PAH
- Most common form of group 3 is due to COPD
Symptoms
– Most common is dyspnea
– Other symptoms include exertional chest pain due to increased myocardial oxygen demand from enlarged right ventricle and increased pressure, peripheral edema, and anorexia (from hepatic congestion)
Diagnostic evaluation
– Transthoracic echo as screening and if evidence of heart disease then likely group 2
– If no evidence of left heart disease then check PFTs, overnight oximetry, VQ scan, LFTs, HIV, ANA, etc to rule out other etiologies of PH
– Patients only need a RHC for confirmation or if other cause of possible PH does not fit the extent of PH seen
– Vasoreactivity testing – if positive then patient would benefit from CCB
– Positive vasoreactivity test is a drop in mPAP of at least 10 and less than 40 mmHg overall without hypotension or drop in CO
Treatment
– For group 2-5 treat the underlying cause
– If evidence of PaO2 < 60 in group 3 then start oxygen
– Treat with anticoagulation to prevent further clots in CTEPH but only definitive treatment is thrombectomy
– For group 1 – can use vasodilators, anticoagulation (because high risk of PE in these patients), digoxin for right heart contractility, and diuretics for volume management
Coccidiomycosis and the Endemic Fungal Infections – 11/13/2017
Gout and Pseudogout – 11/09/2017
SCVMC IM Chief Resident Blog 