Family Medicine Board Review

The rhythm strip shows evidence of sinus tachycardia. This patient has signs of alcohol withdrawal and appropriate management of his hypertension and tachycardia would be to treat his withdrawal with lorazepam. There is no benefit to beta blockers in the management of hypertension and tachycardia related to alcohol withdrawal. The bigger challenge here is to recognize that all tachycardias are not necessarily due to a primary cardiac etiology.

Reference:

Bernstein E, et al. Alcohol and other drugs of abuse. In: Tintinalli JE, et al, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. 2011.

Educational Objective:

Advanced mitral stenosis can cause pulmonary insufficiency as a consequence of pulmonary hypertension.

Key Point:

When mitral stenosis progresses, pulmonary hypertension may develop and consequently pulmonary valve insufficiency. Clinically this manifests as diastolic decrescendo murmur, the Graham Steell murmur.

Explanation:

In advanced mitral stenosis, the originally loud S1 may become soft. The classical low-pitched diastolic rumble of mitral stenosis can be inaudible with a low resting cardiac output. Graham Steell murmur is a diastolic soft blowing decrescendo murmur of pulmonary insufficiency, which appears as the pulmonary hypertension eventually develops later in the course of mitral stenosis.

References:

Carabello BA. Valvular Heart Disease. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Saunders; 2011:453-463

Kosowsky J and Takhar S. Infective Endocarditis and Valvular Heart Disease. Rosen's Emergency Medicine, Chapter 83, 1106-1112.e1

MacIver DH, Adeniran I, MacIver IR, Revell A, Zhang H. Physiological mechanisms of pulmonary hypertension. Am Heart J. 2016 Oct;180:1-11.

Of the above choices, the best prevention for contrast-induced nephropathy is isotonic saline 12 hours prior to the intended dye procedure. Normal saline has been found to be superior to half-normal saline in terms of its enhanced ability in intravascular volume expansion. It also delivers more sodium to the distal nephron and prevents renin-angiotensin activation, and thus maintains increased renal blood flow. In terms of route of administration, oral fluids, while beneficial, are not as effective as intravenous hydration.

The data concerning acetylcysteine are mixed at best, with the level of evidence being a grade 3 according to the American College of Cardiology. In clinical practice, though, NAC therapy remains part of the standard of care because of its low cost, lack of adverse effects, and potential beneficial effect, as demonstrated by the relative risk reduction of CIN, ranging from 0.37-0.73, as reported in several meta-analyses.

Interesting, a 2015 meta-analysis concluded that overall, hydration with sodium bicarbonate (!) could significantly reduce CIN and the length of hospital stay compared with sodium chloride. In addition, NAC added as a supplement to sodium bicarbonate could increase prophylactic effects against nephropathy. The meta-analysis found that hydration with sodium bicarbonate was more effective in emergency coronary imaging and high-risk patients than in elective coronary imaging.

The use of a diuretic such as furosemide is discouraged prior to a cardiac intervention because volume depletion is a risk factor for dye nephropathy. Other associated risk factors include diabetes mellitus, CKD, and multiple myeloma.

References:

Bansal R. Contrast-Induced Nephropathy. updated Jan 18, 2016; accessed November 3, 2016

KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012; 2:8

Calabro P, Binachi R, Crisci M, et al. Use and efficacy of saline hydration and N-acetyl cysteine to prevent contrast-induced nephropathy in low-risk populations undergoing coronary artery angiography. Intern Emerg Med. 2011;6(6):503-507.

Maioli M, Toso A, Leoncini M, et al. Sodium bicarbonate versus saline for the prevention of contrast-induced nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. J Am Coll Cardiol. 2009;52(8):599-604.

Ali-Hassan-Sayegh S, Mirhosseini SJ, Rahimizadeh E, Ghodratipour Z, Sarrafan-Chaharsoughi Z, Dehghan AM, et al. Current status of sodium bicarbonate in coronary angiography: an updated comprehensive meta-analysis and systematic review. Cardiol Res Pract. 2015. 2015:690308.

Friedewald VE, Goldfarb S, Laskey WK, et al. The editor's roundtable: contrast-induced nephropathy. Am J Cardiol. 2007 Aug 1. 100(3):544-51.

The antibody to native double-stranded DNA (anti-dsDNA) test is very specific to systemic lupus erythematosus, as is the antibody to Sm nuclear antigen (anti-Sm) antibody test. They are helpful in confirming the disease. Anti-dsDNA is present in 70% of people with lupus, but in only 0.5% of the general population. The levels of anti-dsDNA in the serum correlate to disease activity.

References:
Rahman A, Isenberg D. Mechanisms of disease: systemic lupus erythematosus. N Engl J Med. 2008;35:8929-39.

Hahn B. Systemic Lupus Erythematosus. In: Longo D et al., eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011:2724-35.

There is a physiological and transient reduction in TSH seen usually between 8 and 14 weeks of gestation. This is due to the thyroid stimulating effects of the physiological increase in hCG in early in pregnancy. In around 20% of women, the TSH may drop below the normal range. After 14 weeks, the TSH usually returns to normal.

Free T4 is an unreliable measure of thyroid status in pregnancy. Due to the increased circulating estrogen levels, there is an increase in thyroid binding globulin (TBG) which first appears in the first half of pregnancy and continues to term. The increase in TBG results in lower levels of free T3 and T4 which stimulates the hypothalamic-pituitary-thyroid axis and results in higher levels of total T3 and T4. In addition, the abundance of deiodinase enzymes found in the placenta result in an increase in the metabolism of T4 to T3.

It is worth noting that even short-term hypothyroidism can pose a risk to this patient; therefore, she should receive appropriate treatment.

References:

Nader S. Thyroid Disease and Pregnancy. Book Chapter in Creasy and Resnik's Maternal-Fetal Medicine: Principles and Practice, 60, 1022-1037.e4

Alexander EK, Pearce EN, Brent GA, Brown RS, Chen H, Dosiou C, Grobman WA, Laurberg P, Lazarus JH, Mandel SJ, Peeters RP, Sullivan S. “2017 Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum.” Thyroid 2017, 27(3):315-389.

Vaidya B, Hubalewska-Dydejczyk A, Laurberg P, Negro R, Vermiglio F, Poppe K. Treatment and screening of hypothyroidism in pregnancy: results of a European survey. Eur J Endocrinol. 2012;166(1):49-54.