Intern Report Case 1.12

intern-report

Presented by Samuel Lee, MD

H&P

A 3 year old African-American male is brought to the ED by his mother with a fever for six days, sore throat, and a rash on his chest.  The patient had been seen by his PCP 3 days ago, diagnosed with scarlet fever, and started on amoxicillin.
Since then the fever has not subsided and the mother has noticed painful swelling and skin peeling over the patient’s lips, palms, soles, and genital area.  The patient cries when walking and avoids placing weight on his soles.  The mother denies any sick contacts.  The patient does not have a cough, nausea, vomiting ,or diarrhea.  He has been eating and drinking, and the mother states that he is still producing urine.

Past Medical History: multiple past ED visits for croup
Medications: Amoxicillin X 3 days
Allergies: None
Immunizations: UTD
Social Hx: lives with mother and grandmother in an apartment
Birth History: Full term SVD

Physical Exam:
Vital Signs: BP 90/56, HR 136, RR 24, Rectal Temp 38.8, Oxygen Sat. 99% on Room air; weight 18 kg
General: The patient is sitting on his mother’s lap; awake and alert, good eye contact; cries if he is made to stand on his feet
HEENT: Atraumatic/normocephalic; PERRL, bilat conjunctival injection, no discharge. The peri-oral area is swollen and erythematous and the lips are cracked. There is pharyngeal erythema with no exudate, vesicles, or lesions seen. MMM. No LAD upon palpation. Neck is supple; there is no nuchal rigidity.
Resp: Lung sounds clear to auscultation. No wheezing/rales/rhonchi.
Chest: Sandpaper rash on chest and upper abdomen which is resolving per mother.  No vesicles or lesions.
CV: RRR, no murmurs, rubs, or gallops; pulses 2+ and equal in all ext.
ABD: Soft, nontender/nondistended.  Positive bowel sounds, no flank tenderness.
EXT: palms and soles are swollen, erythematous, tender to palpation. No vesicles or lesions present. Cap refill less than 2 sec.
GU: There is an erythematous rash and peeling skin on the groin and penis. Testes descended.
Neurological: Awake, alert; able to ambulate but cries when weight is placed on soles.

Impression: Three year old male with 6 day hx of fever and scarlitiniform rash, initially diagnosed as scarlet fever; Condition has not improved with amoxicillin. Now with conjunctival injection, erythema and skin peeling of lips, palms, and GU area.

Lab studies
CBC: WBC 10, Hemoglobin 11.2, Hematocrit 32.6, Platelets 328
Diff: Neutrophils 61%, Lymphocytes 22%, Monocytes 14%, Eosin 3%, Bands 1%
Electrolytes: Na 138, K 4.8, Cl 103, CO2 20, AG 15
BUN 5, Creatinine 0.4
Glucose 110
CRP 75
UA: clear, yellow, Specific Gravity 1.016, pH 7.5, WBC 5-10, no RBC, Nitrite and LE negative; 0 bacteria
CXR: mild hyperinflation, no focal opacity
Rapid Strep test neg
EKG: NSR@100 bpm, no axis deviation, no PR prolongation, no QRS widening, no atrial or ventricular hypertrophy, no ST changes, no T wave inversions, no accessory waves or ectopic beats; no previous EKG available for comparison

QUESTIONS:

1. Given this patient’s history and physical exam, what is the best definitive course of action?

a. Admit the patient for treatment and arrange for an echocardiogram
b. Continue supportive treatment as an outpatient and have the patient follow up in one week for an echocardiogram
c. Initiate antibiotic treatment for Urinary Tract infection and arrange for a voiding cystourethrogram
d. Advise the patient’s mother to continue with amoxicillin and follow up with her PCP in 2 days.

2. What is a serious complication of this patient’s diagnosis?

a. Development of meningitis in the next week
b. Coronary artery aneurysm and myocardial infarction
c. Pyelonephritis
d. Rhabdomyolysis and acute renal failure

3. What is the definitive treatment for this patient’s condition?

a. IV fluid 20cc/kg bolus
b. Nitrofurantoin 2 mg/kg PO X 10 days
c. IVIG 2 mg/kg over 12 hrs, Aspirin 100 mg/kg/day divided qid
d. Acetaminophen 15 mg/kg

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.

Intern Report Case Discussion 1.11

intern-report

Presented by Michael Fernandes, MD

Chief Complaint: “I’m having trouble breathing.”

History of Present Illness:
This is a 46 year-old female presents to the emergency department as a medical code.  Her primary complaint is severe shortness of breath.  She is fully alert, complaining that her breathing has been getting progressively worse, as well as feeling her heart beating inside her chest.  She has also been experiencing progressive swelling of her extremities and abdomen, and significant weakness and fatigue causing her to have difficulty “getting around”.  The duration of these symptoms has been for the past 4-5 months with progressive worsening; today being the worst that she has felt.  She had her family call the ambulence to bring her to the emergency department.  In the ED, she denies any chest pain or chills.  She does admit to having a nonproductive cough with no hemoptysis, and state she is feeling warm, but with no distinct fever.  She has no other acute complaints at this time.

Past Medical History: Negative for hypertension, diabetes, or coronar artery disease
Past Surgical History: Laparoscopic cholecystectomy in 2002
Medications: Denies
Allergies: NKDA
Social History: She denies any drug use.  She does admit to smoking ½ pack of cigarettes every 2 days, and consumes alcohol socially.
OB/GYN History: G3P3003.  Her last menstrual period was 4/22/09.
Family History: Significant for unspecified heart disease; however, she is not aware of any MI, strokes, or diabetes.

Physical Exam:
Vital Signs: BP: 161/94, P: 192, RR: 32, T 38.3, SpO2: 93% on RA
General: Pt appears her stated age.  She is propped up on the stretcher in moderate respiratory distress
HEENT: Head is Normocephalic, atraumatic.
Eyes: Appear to be slightly proptotic, PERRLA, EOMI, sclerae is anicteric, no conjunctival pallor.
Ears: TM are clear, no hemotympanum bilaterally.
Nose: MMM, no erythema, no swollen turbinates, no rhinorrhea or discharge.
Mouth and Throat: MMM, no erythema, no tonsillar exudates, no intraoral lesions.
Neck: Supple, no lymphadenopathy, trachea is midline, carotids are 2+, however, there is significant JVD with the patient sitting upright with the head of the bed at an angle of approximately 85 degrees.
Lungs: Decreased breath sounds on the right, clear on the left.  No wheezing, rhonchi, or rales.  She had significant use of her accessory muscles.  She appears to be acutely dyspneic, however, no cyanosis, no diaphoresis.  She also has dullness to percussion on the right lung base posteriorly.
Cardiovascular: Irregularly, irregular rhythm with a tachycardic rate, unable to appreciate any murmurs, rubs or gallops due to the rapid rate, peripheral pulses are 2+ and symmetric in all 4 extremities.
Abdomen: Firm, markedly proturberant.  Normoactive bowel sounds.  Non-tender, with shifting dullness.  No discernable organomegaly, guarding, or rebound.
Extremities: FROM, strength is 5/5 proximately and distally in both upper and lower extremities.  She has marked dependent pitting edema bilaterally in her lower extremities.
u Feels warm and moist to the touch.  No rashes, no lesions.
Neurological: AAO x3, normal speech and hearing, face is symmetrical.  Sensation is equal and intact throughout.  She has no gross focal motor deficits.

Labs:
Lytes: Na:142 K:4.2 Cl:101 CO2:26 BUN:18 Cr:0.8 Glu:123
Ca:9.1 Mg:2.1 Phos:3.5
CBC: WBC:13,200 Hgb:13.9 Plt:372,000
Coags: PT:11.6 INR:1.04 PTT:24.2
LFTs: WNL Albumin:2.8
SDS: negative
ABG: pH:7.46  PCO2:34  PO2:61  O2 sat:87.2%
Tropnin I: <0.02
TSH: <0.002
BNP: 1232

CXR:

xray1EKG:

EKG1

Questions:

1.    What is the primary medical problem with this patient?
a.    cardiac tamponade
b.    congestive heart failure
c.    hypertensive crisis
d.    pulmonary embolism
e.    thyrotoxicosis

2.    Which agent will block the release of stored thyroid hormone?
a.    furosemide
b.    methimazole
c.    propranolol
d.    propylthiouracil (PTU)
e.    saturated solution of potassium iodide (SSKI)

3.    Which of the following groupings of medications represents the proper treatment sequence?

a.    propanolol, PTU or methimazole, SSKI
b.    propanolol, PTU, SSKI, methimazole
c.    propanolol, SSKI, PTU, methimazole
d.    propanolol, SSKI, PTU or methimazole
e.    SSKI, PTU or methimazole, propanolol

Answers:

1.    E  Thyrotoxicosis
As previously stated, thyrotoxicosis refers to a hypermetabolic clinical syndrome resulting from elevation in serum thyroid hormone, specifically free (T4), (T3), or both.  Hyperthyroidism is one form of thyrotoxicosis where accelerated thyroid hormone biosynthesis and secretion by the thyroid gland produce the clinical syndrome of thyrotoxicosis. The presence of clinical features such as, tachycardia, tremor, eyelid lag, and warm moist skin in a patient with weight loss, difficulty climbing stairs (fatigue and dyspnea), palpitations, and intolerance of warm temperature are all symptoms pathognomonic for thyrotoxicosis.
2.  E saturated solution of potassium iodide (SSKI)
Saturated solution of potassium iodide (SSKI), is necessary to block the release of stored thyroid hormone.  Administration of iodide causes temporary inhibition of iodide organification.  High intrathyroidal iodide concentration is the crucial factor inducing this response.  Thyrotoxic patients are especially sensitive to this effect.   The thyroid uptake of 131I is acutely depressed in thyrotoxic patients by administration of 2 mg potassium iodide, whereas more than 5 mg is needed to depress uptake in normal subjects. Concentrations of serum iodide above 5 µg/dl block binding in the thyrotoxic gland.  It should be administered 1 hour after PTU to ensure that exogenous iodide is not taken up and used to make more thyroid hormone.
3.  A Propanolol, PTU or methimazole, SSKI
Propanalol blocks the activity of the nerves which form the sympathetic nervous system. Overactivity of the sympathetic nervous system is responsible for many of the symptoms of thyrotoxicosis which are “dampened down” by treatment with Propranolol. These include rapidly beating heart (palpitations), shakiness (tremor), intolerance to heat and sweating, diarrhoea, muscle aches and mental symptoms.  PTU, exerts its actions by decreasing thyroid hormone synthesis, and by blocking the conversion of thyroxine (T4) to triiodothyronine (T3).   While  methimazole works, as does PTU, to reduce the levels of thyroid hormone by decreasing thyroid hormone synthesis. In contrast to PTU, methimazole does not significantly inhibit T4 to T3 conversion. Iodide, although it is taken up by the thyroid and used to make thyroid hormone, it can paradoxically suppress release of thyroid hormones from the thyroid gland for several days. Thus, in some patients with severe hyperthyroidism, iodide may be administered to try and shut off stored thyroid hormone release after PTU or methimazole has been started.

Discussion:

Thyrotoxicosis refers to a hypermetabolic clinical syndrome resulting from elevation in serum thyroid hormone levels, specifically free thyroxine (T4), triiodothyronine (T3), or both. Hyperthyroidism is one form of thyrotoxicosis where accelerated thyroid hormone biosynthesis and secretion by the thyroid gland produce the clinical syndrome of thyrotoxicosis.  However, hyperthyroidism and thyrotoxicosis are not synonymous.  In some patients thyrotoxicosis is caused by hyperthyroidism, but other patients may have thyrotoxicosis caused by inflammation of the thyroid gland, which can cause release of stored thyroid hormone (not accelerated synthesis), or by the ingestion of exogenous thyroid hormone.  Differentiating between thyrotoxicosis caused by hyperthyroidism versus other etiology is important because disease management and therapy differs.  Thyroid imaging and radiolabeled tracer thyroid uptake measurements combined with serologic data enable specific diagnosis and appropriate patient treatment.

The clinical features of thyrotoxicosis are mostly independent of its cause.  The presence of tachycardia, tremor, eyelid lag, and warm moist skin in a patient with weight loss, difficulty climbing stairs (fatigue and dyspnea), palpitations, and intolerance of warm temperature are clinical signs and symptoms pathognomonic for thyrotoxicosis.  Elderly patients may have fewer symptoms and limited signs of disease; presenting only with atrial fibrillation, lethargy, or weight loss.  The acute presentation or exacerbation of these signs or symptoms may indicate the onset of thyroid storm, a potentially fatal condition that requires immediate recognition and treatment.

The thyroid gland actively transports iodide from circulating blood into the thyroid follicular cells. Subsequently, iodide is organified into tyrosyl residues of thyroglobulin and stored within the thyroid follicles.  When required, thyroglobulin undergoes proteolysis with the release of T3 and T4 as the principle active forms of thyroid hormone.  In extrathyroidal tissues, some of the T4 is deiodinated to the more metabolically potent T3 hormone.

The process of synthesis, storage, and release of T3 and T4 by the thyroid is normally controlled by the pituitary gland through its release of thyroid stimulating hormone (TSH), also known as thyrotropin.  This process involves a negative feedback loop wherein increasing blood levels of T3 and/or T4, inhibit release of thyrotropin-releasing hormone (TRH) from the hypothalamus and TSH (thyrotropin) from the pituitary.

Management  includes five components:
Supportive care, blockade of peripheral effects, inhibition of thyroid hormone synthesis, slowing of thyroid hormone release, and treatment of the precipitating cause.

1.    Supportive care includes the ABCs, treatment of fever, and, if necessary, treatment of arrhythmias (e.g., atrial fibrillation) with antidysrhythimic agents.  A diuretic such as furosemide may be required for the treatment of pulmonary edema.

2.    Blockade of the peripheral effects of thyroid hormone is crucial in the treatment of thyroid storm. Propranolol is recommended at an adult dose of 1 to 2 mg IV q5 minutes until control of clinical symptoms is achieved.  For patients with conditions such as COPD, asthma, or CHF, a shorter acting and more easily titratable beta-blocker may be preferred, such as esmolol or metoprolol.

3.    Inhibition of thyroid hormone synthesis is achieved with a class of drugs known as thionamides, that include propylthiouracil (PTU) or methimazole.  These drugs prevent hormone sythesis by interfering with the iodination of tyrosine within the colloid of the thyroid follicle.  However, they do not prevent the release of stored thyroid hormone.  The onset of action is within 1 hourr and the full therapeutic effect may take several hours.

4.    Iodide, in the form of saturated solution of potassium iodide (SSKI) or Lugol’s solution, is necessary to block the release of stored thyroid hormone.  It should be administered 1 hour after PTU to ensure that exogenous iodide is not taken up and used to make more thyroid hormone.  Lithium can be an alternative in patient with allergy to iodide.

5.    Glucocorticoids reduce T4-to-T3 conversion, and may have a direct effect on the underlying autoimmune process when the etiology is Graves’ disease.  Their use for the treatment of thyroid storm appears to have improved outcome in at least one study series.  It is acceptable to administer hydrocortisone 100 mg IV every eight hours in patients with thyroid storm; in contrast, glucocorticoids are not routinely used in patients with symptomatic, but not life-threatening, hyperthyroidism.

In patients in whom clinical deterioration occurs despite appropriate therapy, removal of thyroid hormone may be attempted through an exchange transfusion, plasmapheresis, or charcoal hemoperfusion.

Clinical Pearls
•    Recognition of the symptoms of thyrotoxicosis as a medical emergency
•    Labs to order, TSH, free T3, T4
•    Beta-blocker (propranolol preferred), if (COPD, asthma, CHF use esmolol or metoprolol); PTU or methimazole; 1 hour after thionamide – Iodide (SSKI or Lugol’s 7% solution)
•    Treat precipitants or underlying causes, DKA, MI, infection, trauma
•    If patient is allergic to Iodide (SSKI or Lugol’s 7% solution) use Lithium

Conclusion of the case:
The patient’s ABG showed some evidence of hypoxemia with a mild respiratory alkalosis, she was placed on 3 L of oxygen by nasal cannula.  The patient’s ECG showed she was in atrial fibrillation with rapid ventricular rate, she was initially started on diltiazem, which did bring down her heart rate, however, only temporarily.  Clinically, it was felt that she was thyrotoxic (TSH < 0.002 with clinical presentation), the diltiazem was discontinued and propanolol was started 2 mg IV times 3 doses for a total of 6 mg.  PTU 800 mg was given by mouth, and approximately 1 hour later she received 5 drops of Lugol’s 7% solution.  MICU was contacted to admit the patient.  The patient also received 100 mg of hydrocotisone IV.  At the time the patient left the ED, her heart rate was 130 bpm and her BP came down into the 110/70 range.  Her condition remained guarded.

The patient was hospitalized for 20 days.  Echocardiogram showed a dilated RV, mild LVH, and severe systolic dysfunction with an estimated EF of 20-25%.  Treatment of atrial fibrillation and CHF included furosemide, metoprolol, diltiazem, digoxin, and coumadin (thromboembolic prophylaxis).  Her hyperthyroidism was treated with PTU 150 mg. three times daily (methimazole may have been a better choice due to its once a day dosing).  Her hospital stay was complicated by a pneumothorax requiring chest tube placement following a diagnostic and therapeutic thoracentesis.  The patient was readmitted in July 2008 for respiratory failure and unfortunately died.

This case discussion presented by Michael Fernandes, MD

Intern Report Case 1.11

intern-report

Presented by Michael Fernandes, MD

Chief Complaint: “I’m having trouble breathing.”

History of Present Illness:
This is a 46 year-old female presents to the emergency department as a medical code.  Her primary complaint is severe shortness of breath.  She is fully alert, complaining that her breathing has been getting progressively worse, as well as feeling her heart beating inside her chest.  She has also been experiencing progressive swelling of her extremities and abdomen, and significant weakness and fatigue causing her to have difficulty “getting around”.  The duration of these symptoms has been for the past 4-5 months with progressive worsening; today being the worst that she has felt.  She had her family call the ambulence to bring her to the emergency department.  In the ED, she denies any chest pain or chills.  She does admit to having a nonproductive cough with no hemoptysis, and state she is feeling warm, but with no distinct fever.  She has no other acute complaints at this time.

Past Medical History: Negative for hypertension, diabetes, or coronar artery disease
Past Surgical History: Laparoscopic cholecystectomy in 2002
Medications: Denies
Allergies: NKDA
Social History: She denies any drug use.  She does admit to smoking ½ pack of cigarettes every 2 days, and consumes alcohol socially.
OB/GYN History: G3P3003.  Her last menstrual period was 4/22/09.
Family History: Significant for unspecified heart disease; however, she is not aware of any MI, strokes, or diabetes.

Physical Exam:
Vital Signs: BP: 161/94, P: 192, RR: 32, T 38.3, SpO2: 93% on RA
General: Pt appears her stated age.  She is propped up on the stretcher in moderate respiratory distress
HEENT: Head is Normocephalic, atraumatic.
Eyes: Appear to be slightly proptotic, PERRLA, EOMI, sclerae is anicteric, no conjunctival pallor.
Ears: TM are clear, no hemotympanum bilaterally.
Nose: MMM, no erythema, no swollen turbinates, no rhinorrhea or discharge.
Mouth and Throat: MMM, no erythema, no tonsillar exudates, no intraoral lesions.
Neck: Supple, no lymphadenopathy, trachea is midline, carotids are 2+, however, there is significant JVD with the patient sitting upright with the head of the bed at an angle of approximately 85 degrees.
Lungs: Decreased breath sounds on the right, clear on the left.  No wheezing, rhonchi, or rales.  She had significant use of her accessory muscles.  She appears to be acutely dyspneic, however, no cyanosis, no diaphoresis.  She also has dullness to percussion on the right lung base posteriorly.
Cardiovascular: Irregularly, irregular rhythm with a tachycardic rate, unable to appreciate any murmurs, rubs or gallops due to the rapid rate, peripheral pulses are 2+ and symmetric in all 4 extremities.
Abdomen: Firm, markedly proturberant.  Normoactive bowel sounds.  Non-tender, with shifting dullness.  No discernable organomegaly, guarding, or rebound.
Extremities: FROM, strength is 5/5 proximately and distally in both upper and lower extremities.  She has marked dependent pitting edema bilaterally in her lower extremities.
u Feels warm and moist to the touch.  No rashes, no lesions.
Neurological: AAO x3, normal speech and hearing, face is symmetrical.  Sensation is equal and intact throughout.  She has no gross focal motor deficits.

Labs:
Lytes: Na:142 K:4.2 Cl:101 CO2:26 BUN:18 Cr:0.8 Glu:123
Ca:9.1 Mg:2.1 Phos:3.5
CBC: WBC:13,200 Hgb:13.9 Plt:372,000
Coags: PT:11.6 INR:1.04 PTT:24.2
LFTs: WNL Albumin:2.8
SDS: negative
ABG: pH:7.46  PCO2:34  PO2:61  O2 sat:87.2%
Tropnin I: <0.02
TSH: <0.002
BNP: 1232

CXR:

xray1EKG:

EKG1

Questions:

1.    What is the primary medical problem with this patient?
a.    cardiac tamponade
b.    congestive heart failure
c.    hypertensive crisis
d.    pulmonary embolism
e.    thyrotoxicosis

2.    Which agent will block the release of stored thyroid hormone?
a.    furosemide
b.    methimazole
c.    propranolol
d.    propylthiouracil (PTU)
e.    saturated solution of potassium iodide (SSKI)

3.    Which of the following groupings of medications represents the proper treatment sequence?

a.    propanolol, PTU or methimazole, SSKI
b.    propanolol, PTU, SSKI, methimazole
c.    propanolol, SSKI, PTU, methimazole
d.    propanolol, SSKI, PTU or methimazole
e.    SSKI, PTU or methimazole, propanolol

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.

Intern Report Case Discussion 1.10

intern-report

Presented by Ryan Phillips, MD

History of present illness:

A 76-year-old female was wheeled down to the first aid station during a 90 degree Thursday afternoon day game at Comerica Park. The patient is a member of an assisted-living home and is visiting the park as a part of “Senior Day” promotion at the assisted living home.   The patient is wheeled down by one of the nurses from the home.  She knows some of the patient’s medical history and knows the patient has been in good health and was her normal alert and orientated self before coming to the baseball park today.  She was sitting enjoying herself for the first few innings, but the patient was thought to be napping for the past three innings.  In the bottom of the 8th inning the patient was noticed to be unresponsive and not napping.  The patient now is not responding to verbal stimuli, which is not normal for her.

Past medical history (as provided by the nurse): hypertension, mentally impaired

Medications: Metoprolol and hydrochlorothiazide

Allergies: NKDA

Past surgical history: Unknown

Social history:  patient lives at a member assisted living home patient does not smoke drink or use any drugs as per the nurse with the patient

Family History: unknown

Review of systems: unobtainable

Physical examination

VS: T 40.5°C oral, HR 140 RR 28 BP 90/60

Gen: patient is obtunded, skin is hot and dry, pt is responding to painful stimuli but not responding to verbal

HEENT: pupils equal and reactive to light, no pallor, anicteric, there are no facial asymmetrys noted, head is normocephalic, atraumatic, nares have no discharge, oral pharynx appears dry, no erythema, + gag, neck is supple, no JVD, trachea midline

Respiratory: patient is tachypneic, lungs are clear to auscultation bilaterally with no expiratory wheeze rales or rhonchi, patient has equal chest rise

CVS: tachycardic with S1-S2 present, no murmurs or rubs

Abdomen: soft, nontender, nondistended, with positive bowel sounds, no masses, no organomegaly appreciated

Extremities: patient able to move all 4 extremities in response to pain, no asymmetric swelling or erythema patient has 1+ pulses bilateral radial and bilateral pedal, slightly decreased but symmetrical muscle tone

Skin: hot and dry, no rashes, no jaundice, no diaphoresis

Neurologically: patient responds to painful stimuli and pupils are equal and reactive to light no facial asymmetry is note, noted to move all 4 extremities, +1 DTRs, no clonus, no cogwheel rigidity

Laboratory studies

CBC Hb – 16, WBC – 12, hematocrit 51 platelets 416

Electrolytes Na – 134 K – 5.1, Cl 96, HCO3 26, BUN 62, Cr 2.1 glucose 90

AST 245 ALT 276

Chest x-ray no acute occult cardiopulmonary process

Question 1

What is this patient most likely diagnosis?

A. Acute renal insufficiency

B. Heat exhaustion

C. Heat stroke

D. Hepatitis

E. Meningitis

Question 2

After controlling ABCs what is your next step in management with this patient?

A. CT of the head followed by lumbar puncture and initiation of steroids, ampicillin, ceftriaxone

B. Exchange transfusion and plasmapheresis

C. Oral hydration with hypotonic solutions

D. Placing an NGT and giving the patient acetaminophen 1,000mg and ibuprofen 800mg via NGT

E. Rapid cooling by removing clothing, misting the patient with water and/or immersing the patient in a tepid water bath

Question 3

Despite the treatment given, the patient declines and requires rapid sequence intubation.  Following successful intubation, the patient develops muscle rigidity, acidosis and her temperature is now 42°C.  What medication is indicated?

A. Atropine

B. Physostigmine

C. Dantrolene

D. Lorazepam

E. Sodium bicarbonate

_________________________________________________________________________________________

Discussion

Question 1

What is this patient most lately diagnosis?

A.Acute renal insufficiency

B.Heat exhaustion

C.Heat stroke

D.Hepatitis

E.Meningitis

This is an elderly patient that was in good health until she sat in the 90 heat for an extended period of time and is now suffering from heat stroke.  Heat stroke is the most severe form of a series of heat related illnesses.  It is a catastrophic life-threatening emergency with multiorgan system involvement and a high mortality rate that requires immediate intervention that occurs when the homeostatic mechanisms fail to alleviate extreme body temperatures usually greater than 40°C.  The classic definition is a core temperature greater than 40°C, anhidrosis and CNS dysfunction.  These criteria, however, are not absolute diagnostic criteria.  Absence of sweating may or may not be present as hyper-hidrosis is followed by anhidorsis, thus, there may still be sweat present at presentation.  CNS dysfunction is not specifically defined, however some alteration of mental status must be present and 40°C is not a diagnostic cutoff.

Prolonged heat stress causes an increase in blood flow via peripheral vasodilation.  As the body tries to release heat at the skin surface, this results in a decrease in blood flow to splanchnic and renal vasculature.  This decreased blood flow results in splanchnic and renal ischemia causing nausea, vomiting and diarrhea.  Further ischemia will cause hepatic damage.  Laboratory studies may show increased renal function and LFTs after prolonged heat exposure.  Further heat stress causes the compensatory splanchnic vasoconstriction to fail causing the core blood temperature to dramatically increase.  This causes elevated intracranial pressure with a reduction of mean arterial pressure leading to decrease cerebral blood flow and major CNS dysfunction.

The most important treatment for heat stroke is rapid cooling as described in answer to Question 2.

Other forms of minor heat related illness

Heat edema

Prickly heat

Heat Cramps

Painful involuntary spasmodic contractions of skeletal muscles usually involving the calves.  Found in individuals sweating profusely causing losses of water or other hypotonic solutions may occur during exercise or more likely rest. Heat cramps are self-limited and do not cause significant morbidity.  The pain of heat cramps do not respond to opiates alone.  Heat cramps are limited to definitive group of muscles and are not known to cause rhabdomyolysis.  Pathogenesis is due to depletion of sodium and potassium at the level of the muscle.  Treatment consists of fluid and salt replacement with oral rehydration or intravenous rehydration in more severe cases.

Heat Syncope

Heat Exhaustion
A dehydration induced heat retention insufficient to cause heat stroke.  It is characterized by a combination of salt depletion and water depletion.  Symptoms include weakness, malaise, lightheadedness, fatigue, dizziness, nausea or vomiting, frontal headache, and myalgias.  Signs in the ER include orthostatic hypotension, sinus tachycardia, tachypnea, diaphoresis and syncope.  The core temperature usually remains below 40°C. Mental status remains normal.  Heat cramps and/or rhabdomyolysis may also be present on rare occasion.  Treatment includes rest, remove the patient from the heat environment, assess volume status and replace fluid.  Choice of intravenous solutions should be guided by laboratory determinations, isotonic salt solutions may be used until specific electrolyte abnormalities are identified.  If there is a free water deficit,  free water should be replaced slowly over 48 hours or correction of hypernatremia associated with seizures caused by cerebral edema.  Patients can be treated as outpatients if appropriate, but may need admission with significant electrolyte abnormalities.

Exhaustion has a potential progress to heat stroke.  The major differences between heat stroke and heat exhaustion are that heat stroke classically involves anhidrosis, CNS dysfunction and core temperature of greater than 40°C.  Typically the degree of dehydration and volume loss is greater with heat exhaustion versus heat stroke.

Question 2

After controlling ABCs what is your next step in management with this patient?

A. CT of the head followed by lumbar puncture and initiation of steroids, ampicillin, gentamicin and metronidazole

B. Exchange transfusion and plasmapheresis

C. Oral hydration with hypotonic solutions

D. Perform synchronized cardioversion at 100 KJ followed by adenosine 6 mg

E. Rapid cooling by removing clothing, misting the patient with water and/or immersing the patient in a tepid water bath

This patient needs to be rapidly cooled.  The patient also needs fluids, but that is independent of rapid cooling.  Several ways are appropriate to reduce a patient’s temperature and the best way to understand how is by understanding the different mechanisms of heat transfer

Evaporation – Heat loss mechanism accounts for over 25% and heat lost in cooler settings and virtually 100% at high environmental temperatures.  Heat loss is impaired at higher levels of humidity as evaporation is impaired.  This method of heat loss is enhanced by misting the patient with water or sponge baths.  Heat is pulled from the patient to help the water evaporate.  Placing a fan on the patient will increase the rate of evaporation and make this method even more effective.

Conduction – Kinetic energy of moving molecules in warm skin is transferred to the less kinetically active molecules in cooler surface. Usually occurs at less than 3% total heat loss of the body, but can be enhanced when ice packs are placed in the patients groin and axilla.  Can also be enhanced by placing the patient in a tepid water bath.  A tepid water bath is used for patient comfort and to prevent patient shivering.

Radiation – Primary mechanism of heat lost when the environmental temperature is lower than the body temperature.  Body heat is lost through infrared range of the electromagnetic spectrum.  When the body heat is less than the environmental temperature the body will gain the infrared heat.  It is best to move the patient a cooler environment

A combination of all four cooling mechanisms should be utilized.  The environment will dictate which mechanism will be the most appropriate.  The most practical method will often be a combination of evaporation and ice bags.  It is important to remember that antipyretics are ineffective and therefore not indicated in a patient with environmental hyperthermia.

Question 3

Despite the treatment given, the patient declines and requires rapid sequence intubation.  Following successful intubation, the patient develops muscle rigidity, acidosis and her temperature is now 42°C.  What medication is indicated?

A. Atropine

B. Physostigmine

C. Dantrolene

D. Lorazepam

E. Sodium bicarbonate

Malignant hyperthermia can be induced in the emergency department after the administration of general anesthesia.  It is rare in the emergency department setting, but it can occur with neuromuscular blocking agents such as succinylcholine and if the person has the inherited muscle disorder.  Malignant hyperthermia causes hyperthermia, muscle rigidity and acidosis and is treated with dantrolene.  Malignant hyperthermia is caused by an instability of skeletal muscle sarcoplasmic reticulum and the release of calcium.  Dantrolene treats malignant hyperthermia by lowering myoplasmic calcium.

Other drug induced hyperthermias include neuroleptic malignant syndrome and serotonin syndrome.  Neuroleptic malignant syndrome symptoms include muscular rigidity, severe dyskinesia, akinesia, tachycardia, dyspnea, dysphagia and urinary incontinence.  It is caused by dopamine receptor blockade from haloperidol or other antipsychotic medications causing muscle spasticity and dystonia.  Treatment starts with withholding neuroleptic agents followed by supportive care against potential complications including dehydration,electrolyte imbalances, rhabdomyolysis, renal failure, cardiac arrhythmias, seizures, hepatic failure and sepsis.

Serotonin Syndrome is a condition associated with increased serotonergic activity in the CNS.  It can be caused by therapeutic medication use, drug interactions or intentional self-poisoning.  Symptoms can range from mild tremor to life threatening hyperthermia.  Other symptoms can include diaphoresis, tachycardia, hypertension, vomiting, diarrhea, tremor, muscle rigidity, myoclonus and hyperreflexia.  Treatment of serotonin syndrome includes discontinuation of all serotonergic agents, supportive care aimed at normalization of vital signs, sedation with benzodiazepines, and administration of serotonin antagonists.

It is important to recognize hyperthermia has a wide differential diagnosis.  This patient had strong clinical presentation for an environmental hyperthermia.  Other diagnoses that need to be in the differential for high fever include sepsis or meningitis, seizures, toxins, CNS hemorrhage, thyroid storm malignant hyperthermia, neuroleptic malignant syndrome or serotonin syndrome.  If the patient responds to rapid cooling and becomes more responsive further workup may be unnecessary.  However, if a person presents from an apartment without air conditioning  in mid-July without any more history available we would be unable to differentiate if this person is hyperthermic from environment versus other etiologies such as infection or ICH.  The infection or ICH may be preventing the patient from leaving the 100 degree apartment.  This patient would need extensive evaluation and treatment to rule out other etiologies such as a head CT and LP.

References

Boyer, E. W. M., PhD (2009) Serotonin Syndrome. UpToDate

Eelco FM Wijdicks, M. (2009) Neuroleptic Malignant Syndrome. UpToDate

Helman, R. S., MD and M. Rania Habal (2007) Heatstroke. eMedicine

Lin, J., MD, MPH, FACEP, M. Ralph Losey, FACEP, et al. (2009) An Evidence-Based Approach to Hyperthermia and Other Heat-Related Emergencies. Pediatric Emergency Medicine Practice 6, 1-16

Marx, J. A., R. S. Hockberger, et al. (2006). Rosen’s emergency medicine : concepts and clinical practice. Philadelphia, Mosby/Elsevier.

Tintinalli, J. E., G. D. Kelen, et al. (2004). Emergency medicine : a comprehensive study guide. New York, McGraw-Hill, Medical Pub. Division.

Intern Report Case 1.10

intern-report

Presented by Ryan Phillips, MD

History of present illness:

A 76-year-old female was wheeled down to the first aid station during a 90 degree Thursday afternoon day game at Comerica Park. The patient is a member of an assisted-living home and is visiting the park as a part of “Senior Day” promotion at the assisted living home.   The patient is wheeled down by one of the nurses from the home.  She knows some of the patient’s medical history and knows the patient has been in good health and was her normal alert and orientated self before coming to the baseball park today.  She was sitting enjoying herself for the first few innings, but the patient was thought to be napping for the past three innings.  In the bottom of the 8th inning the patient was noticed to be unresponsive and not napping.  The patient now is not responding to verbal stimuli, which is not normal for her.

Past medical history (as provided by the nurse): hypertension, mentally impaired

Medications: Metoprolol and hydrochlorothiazide

Allergies: NKDA

Past surgical history: Unknown

Social history:  patient lives at a member assisted living home patient does not smoke drink or use any drugs as per the nurse with the patient

Family History: unknown

Review of systems: unobtainable

Physical examination

VS: T 40.5°C oral, HR 140 RR 28 BP 90/60

Gen: patient is obtunded, skin is hot and dry, pt is responding to painful stimuli but not responding to verbal

HEENT: pupils equal and reactive to light, no pallor, anicteric, there are no facial asymmetrys noted, head is normocephalic, atraumatic, nares have no discharge, oral pharynx appears dry, no erythema, + gag, neck is supple, no JVD, trachea midline

Respiratory: patient is tachypneic, lungs are clear to auscultation bilaterally with no expiratory wheeze rales or rhonchi, patient has equal chest rise

CVS: tachycardic with S1-S2 present, no murmurs or rubs

Abdomen: soft, nontender, nondistended, with positive bowel sounds, no masses, no organomegaly appreciated

Extremities: patient able to move all 4 extremities in response to pain, no asymmetric swelling or erythema patient has 1+ pulses bilateral radial and bilateral pedal, slightly decreased but symmetrical muscle tone

Skin: hot and dry, no rashes, no jaundice, no diaphoresis

Neurologically: patient responds to painful stimuli and pupils are equal and reactive to light no facial asymmetry is note, noted to move all 4 extremities, +1 DTRs, no clonus, no cogwheel rigidity

Laboratory studies

CBC Hb – 16, WBC – 12, hematocrit 51 platelets 416

Electrolytes Na – 134 K – 5.1, Cl 96, HCO3 26, BUN 62, Cr 2.1 glucose 90

AST 245 ALT 276

Chest x-ray no acute occult cardiopulmonary process

Question 1

What is this patient most likely diagnosis?

A. Acute renal insufficiency

B. Heat exhaustion

C. Heat stroke

D. Hepatitis

E. Meningitis

Question 2

After controlling ABCs what is your next step in management with this patient?

A. CT of the head followed by lumbar puncture and initiation of steroids, ampicillin, ceftriaxone

B. Exchange transfusion and plasmapheresis

C. Oral hydration with hypotonic solutions

D. Placing an NGT and giving the patient acetaminophen 1,000mg and ibuprofen 800mg via NGT

E. Rapid cooling by removing clothing, misting the patient with water and/or immersing the patient in a tepid water bath

Question 3

Despite the treatment given, the patient declines and requires rapid sequence intubation.  Following successful intubation, the patient develops muscle rigidity, acidosis and her temperature is now 42°C.  What medication is indicated?

A. Atropine

B. Physostigmine

C. Dantrolene

D. Lorazepam

E. Sodium bicarbonate

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.

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