Inter Report Case Discussion 1.9

intern-report

Presented by Mondeep Narewal, MD

HPI:
A 55-year-old man presents to the ED for progressive shortness of breath. His past medical history is significant for congestive heart failure, chronic obstructive pulmonary disease, diabetes hypothyroidism, and kidney failure.   Only a limited history could be obtained as the patient is short of breath.  He states that he has been getting short of breath for the past week.  He also states that he has had some increased swelling in his feet and hands.  He usually is on  home oxygen  however has noted he needs more now.
Pt states he has had a cough and sputum production but no changes from baseline.
He has three pillow orthopnea and PND.  Patient states he has been compliant with all medications.

A review of his medical record shows that the patient was admitted 2 weeks prior for progressive shortness of breath secondary to CHF and it is noted that he has a dilated cardiomyopathy.  His ecocardiogram during this admission revealed an ejection fraction of 45%.

ROS: (limited secondary to shortness of breath)

He states he is fatigue and feels cold over his body.  Denies any chest pain, diaphrosis, palpitations.  No vomiting, no dizziness.  He states that he has been slightly more constipated than usual.  No blood per rectum.  No diarrhea.

PMH:
CHF, COPD, DM, hypothyroidism and chronic renal insufficiency

Medications:
Carvedilol, levothyroxine, , insulin, albuterol, sprivia, ASA

Allergies:NKDA

Social:
Positive for smoking history, no crack or cocaine or drug use.  Denies any ETOH.

Physical Exam:

VS:  T=35.1 Oral, HR=67, RR=28 BP=138/94 O2 Sat=87% on 2 L
General:  Pt  has a significant conversational dyspnea and appears in mild to moderate respiratory distress
Face:  Symmetrical simile no focal deficits has some non-pitting edema around the eyes.
Eyes: Conjunctiva pale, PERRLA, EOMI,
Ears: Clear TM
Mouth:  Slightly enlarged tongue no erythema no exudates.
Neck: Supple, enlarged thyroid gland that is non tender, no bruits heard, there is a JVD 7cm, trachea midline
Cardiac:  normal S1 and S2, has an S3,no murmurs, no rubs, regular rhythm
Lungs: Rales at both bases, wheezing diffusely throughout both lung fields.
Abd: Obese, soft, NTND, no rebound no guarding.
Extremities: Pulses symmetrical 2+ throughout, 2+ edema pitting in lower legs.
Neuro Exam:  Patient has no focal deficits, CN II-X12 (8 not tested) grossly intact.
Patient’s strength is 5/5 moving all extremities, has decreased reflexes at both patella and biceps but symmetrically decreased no clonus.
Skin Exam:  Dry cool skin, patient feels cool to the touch, cap refill is slightly prolonged, there is no erythema or lesions.

Lab Results:
CBC:  H/H 13/39, WBC: 12, Plt 190
Lytes:  132/4.4/107/26/2.5  Glucose=140
UA:  Negative
Troponin <0.02
Mg 2.1
TSH:  50 uIU/ml

EKG: NSR, Slightly flattened T waves, no ST depression or elevation,  prolonged QTc interval

CXR: Pulmonary congestion with b/l pleural effusions no cardiomegaly.

Questions:

1.  Taking the patient’s presenation into consideration, which of the following is the most likely diagnosis?
a)    Sepsis
b)    Congestive heart failure
c)    COPD exacerbation
d)    Hypothermia
e)    MI

2.  Given the patients clinical presentation and lab results what would be the most likely reason that this patients underlying condition has worsened?
a)    MI
b)    Uncontrolled Diabetes
c)    Pneumonia
d)    Noncomplaince with medications
e)    Thyroid function

3.  Given this patient’s clinical presentation, what is the most appropriate immediate management?

a)    Supplement O2, furosemide, nitroglycerin
b)    Supplement O2, steroids, albuterol atrovent
c)    Supplement O2, beta-blockers, furosemide
d)    Supplement O2, furosemide, nitroglycerin, start low dose levothyroxine
e)    Supplement O2, furosemide, nitroglycerin, start high dose IV levothyroxine replacement

Discussion:

Acute decompensated heart failure is one of the most common medical problems encountered in the emergency department.  This is a clinical syndrome of dyspnea, elevated cardiac filling pressures and neuro-hormonal elements leading to increasing fluid retention activated by the rennin-anigotensin system.  The spectrum of acute decompensated heart failure ranges from dyspnea with activity to cardiogenic shock.

Often patients with known congestive heart failure present with pulmonary complaints of increasing dyspnea and swelling in their legs. However, the underlying clinical presentation can be quite variable depending on the patients cause of heart failure.  Patients with preserved systolic ejection fractions (i.e. diastolic failure) in the acute setting of heart failure often present with less obvious clinical symptoms than those with systolic failure.  The homeostatic effects of maintaining cardiac output lead to changes in the systemic vascular resistance; affected largely by the hormonal components of fluid retention and increasing heart rate.

In the emergency room it is more important to identify heart failure as the cause of a patients dyspena than the underlying cause of the disease expect in cases where the heart failure can potentially be reversed by treating the underlying etiology of the disease.

The thyroid’s involvement in heart failure is often overlooked in the emergency department in favor of stabilizing and managing the critical patient.  While hypothyroidism contributes to a small fraction of patients with heart failure, it is an important screening test as it is a reversible cause of heart failure and early treatment has the potential to reduce hospitalization time and improves outcomes.   One study showed1 that those patients with subclinical hypothyroidism when compared to euthyroid patients had a moderately increased risk of developing heart failure over a 12-year span.

As a result, idenitifying patients at risk of heart failure and hypothryodism can potentially decrease hospital visits for congestive heart failure.  Patients often present with increased swelling of extremities, complaints of cold intolerance, bowel constipation, increase generalized fatigue, weight gain, and mood disturbance.  Women are more commonly affected than men.  Autoimmune disease is the most often cause of hypothyroidism in patients.  While screening for hypothriodism in the ED is not routine it may be of benefit in patients with increased risk factors for both hypothyroidism and congestive heart failure.

The effects of low thyroid hormone on the cardiovascular system are from a deficiency of thyroxine on heart function.  This leads to a reduction in heart rate and in severe cases, a lower blood pressure.  In a patient with acute heart failure and hypothyroidism, the adaptive mechanisms are impaired leading to a worsening or more severe presentation of heart failure. The lack of thyroxine leads to a global hypokinesis of the heart (which maybe reversible) and reduced heart function.  With prolonged hypothyroidism often an increase in serum cholesterol levels are observed.  This increase in serum cholesterol makes hypothyroidism an indirect risk factor for coronary artery disease.  As such, a patient with an under active thyroid is at an increased risk for ischemic heart disease.  Patients may present with elevated TSH (0.5-5.0 mIU/L normal), or hypothermia with EKG changes consistent with ischemia, prolonged QT interval , sinus bradycardia, pericardial effusion, AV block, or atrial fibrillation can all be present.

Another lesser complication complication of hypothyroidism in congestive heart failure is the presence of pericardial effusions that may lead to cardiac tamponade.

Answers:

Question 1: The answer is B

This patient’s history, physical and lab values all are most suggestive of congestive heart failure.  The patient describes an increasing shortness of breath that has worsened over the last few days, now requiring more oxygen. He has also noted an increase in swelling.  He also describes three-pillow orthopnea with PND.  His physical exam finds are consistent with a fluid overload state, including JVD, B/L rales, and edema in his extremities.  His chest x-ray is consistent with congestive heart failure given the presence of pulmonary congestion and B/L pleural effusions.  While the presence of cardiomegaly on cxr would be more suggestive of heart failure, however, a normal cardiac silhouette on x-ray does not rule out cardiomyopathy related heart failure.  The lower than expected heart rate in this patient can be attributed to either is beta blockade or his hypothyroidism disease.

(A) is incorrect –  while the patient  meets SIRS criteria, T < 36 , and tachypnea R > 20, he does not have a white blood cell count greater than 12,000, his HR is less than 90 beats per minute and most importantly there is no source to define this as sepsis.  (C) is incorrect, while his COPD may be an exacerbating factor for decompensated heart failure, he notes that his cough and sputum production is at baseline.  He has had no fever to suggest infection.  (D) is incorrect – while the patient’s temperature is in fact lower than average, patients at temperatures around 35C are in stage one of hypothermia.  They often only require external warming procedures.  The hypothermia is unlikely to be severe enough to cause myocardial depression leading to heart failure.   (E) is unlikely.  Myocardial infraction can cause decompensated heart failure, however, the patient does not have any chest pain, diaphoresis, or palpitations suggestive of a MI, his EKG does not show any ST segment changes nor are his cardio biomarkers positive.

Question 2: The answer is E.

While all the above can cause worsening symptoms in patients with congestive heart failure – the history, labs and clinical findings are most consistent with hypothyroidism.  His TSH is noted to be 50 uIU/mL with the normal range between 0.5 to 5.0 uIU/mL.  The lack of thyroid hormone causes a global hypokinetic heart leading to worsening of heart failure.

Question 3:  The answer is D.

This patient presents with acute decompensated heart failure, most likely moderate failure.  The goals are to reduce cardiac workload by decreasing preload and afterload and improving cardiac output.  The use of supplemental oxygen is required if the patient is hypoxic, and in severe cases the use of BiPap allows adjustments to be made to the PEEP that can lead to a drop in preload.  Nitrates are useful to decrease the preload and afterload in this patient.  His blood pressure appears to be able to tolerate the use of nitrates as he is not hypotensive at this point.  Furosemide is useful in symptomatic relief over time and diuresis of the patient allows for breakage of the rennin-angiotensin and neuro-hormonal cycle of fluid retention in CHF to be addressed.  However, this patient has underlying renal insufficiently so the effectiveness of furosemide may be limited.    Beta blockers, while not always an absolute contraindication in CHF patients in the acute phase, several papers have been published with regards to the effects and usage in patients with chronic beta blocking therapy and normal blood pressure states, they are most useful in diastolic rather systolic dysfunction.  However, in the ED it is often difficult to asses a patient has purely having diastolic or systolic dysfunction and most choose to avoid the use of beta blockers in acute heart failure patients.

In patients with low thyroid function leading to decrease cardiac output, replacement therapy should be titrated towards a euthryoid state rather than having high dose thyroid hormone replacement.  The reason is simple, high dose replacement leads to an increase oxygen demand on the heart in patients have already have an increased risk for coronary artery disease.  The end result is an increase potential to induce an MI.  The only clinical presentation where rapid administration of levothyroxine is warranted is in patients with myxedema coma.

This case discussion presented by Mondeep Narewal MD

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