Senior Report 7.7

Case Presentation by Dr. Adnan Sabic, MD

CC: I don’t feel well

HPI: Fifty seven year old female presents complaining of not feeling well since this morning. Patient complains of feeling dizzy, however denies feeling lightheaded. Patient denies passing out. She denies any chest pain, shortness of breath, nausea or vomiting. She does report few episodes of watery diarrhea early this morning. She does not have any other complaints.

PMH: HTN, HLD and ESRD on HD and was dialyzed 2 days ago and is due tomorrow

Examination:
Vital signs: BP 70/36, HR 32, RR 13, Temp 36.7, Pulse Ox 96% on room air
General: Patient is laying in bed, eyes closed, however easily arousable and answering questions appropriately
Eyes: PERRL, no conjunctival pallor
Neck: No JVD
Cardiac: Bradycardic, no murmurs appreciated
Respiratory: LCTAB
GI: Abdomen is soft, NT/ND
Msk: Fistula present in left upper extremity. No overlying redness.
Skin: Warm and dry
Neurological: Awake and moving all extremities spontaneously. No facial droop. Pupils are equal, round and reactive to light. Strength is 5/5 in upper and lower extremities bilaterally.

 

Following ECG was obtained:

adnan

Questions:

  1. Based on this patient’s presentation, what is the most likely to be her primary disorder?
    1. Hypocalcemia
    2. Hyperkalemia
    3. Hypemagnesemia
    4. Hypokalemia
  1. What is the best initial treatment for this patient?
    1. Calcium Gluconate 1 gm IVP
    2. NaHCO3 1 AMP IVP
    3. Atropine 0.5 mg IVP
    4. Albuterol 5 mg nebulized treatment
  1. What is the onset and duration of action of the drug that was administered in question 2?
    1. 1-5 minutes and lasts for 60 minutes
    2. 10-50 minutes and lasts for 6 hours
    3. 1 hour and lasts for 16 hours
    4. 2 hours and lasts for 24 hours

 

Answers & Discussion:

1)    2
2)    1
3)    1

Hyperkalemia is a very common presentation seen in the emergency departments across the country. Vast majority of the presentations are benign and most of the patients have no complications from it. However, hyperkalemia can be very serious and it can lead to death.

Hyperkalemia is defined as potassium greater than 5.5 mEq/L. Hyperkalemia is especially important in patients who are dialysis dependent. Usually ESRD patients are able to tolerate higher levels of potassium, however in patients who receive dialysis regularly, even potassium of 6.0 mEq/L can lead to severe presentations.

Most patients with hyperkalemia will be asymptomatic, however patients can present with generalized malaise, shortness of breath and in cardiac arrest. It is critical for ED physician to consider hyperkalemia in cardiac arrest in ESRD patients. In ESRD patients, it is imperative to obtain an ECG in any patient who presents with weakness, feeling short of breath, syncope or any other presentation that can be caused by hyperkalemia.

ECG changes associated with hyperkalemia have sequential progression. Patients with serum potassium levels of 5.5-6.5 mEq/L will usually have peaked tall T waves and shortened QT interval and possibly ST segment depression. Serum potassium level of 6.5-8.0 mEq/L will present with prolonged PR interval, decreased or disappearing P waves and widening of QRS. Levels higher than 8.0 mEq/L will have progressive QRS widening, bradycardia and absent P waves, which will lead to sine wave and eventuall ventricular fibrillation or asystole.

Patients who present with symptomatic hyperkalemia, should be evaluated in the resuscitation bay. IV access should be established as soon possible and patient should be placed on continuous cardiac monitoring. An ECG should be immediately obtained. If the ECG shows signs of hyperkalemia then treatment should be initiated immediately.

  • The first IV therapy should be calcium. Hyperkalemia causes irritation of cardiac membranes and this should be immediately treated with calcium gluconate or calcium chloride. Calcium gluconate can be administered thru the peripheral line. Calcium chloride should be administered thru central line. At least 1 gm of calcium gluconate or chrloride should be administered. Because of the short duration of action, definitive treatment should be initiated as soon as possible.
  • Insulin can be administered as well, which promotes intracellular movement of potassium. Five to 10 units of regular insulin should be administered.
  • Glucose should be supplemented too if the patient is euglycemic with D50.Frequent glucose checks should be ordered since insulin is metabolized by kidneys and in ESRD patients this can cause prolonged half life which can cause hypoglycemia.
  • Albuterol is an adjunctive treatment. It can be started while IV access is being established or during the process of obtaining the IV. Albuterol nebulized treatment, 5-10 mg. Albuterol shifts potassium into the cells which can last up to 2 hours.

HyperkalemiaTable

Hemodialysis is the definitive treatment for hyperkalemia and it should be initiated as soon as possible. Kayexalate can be administered as well, however according to some of the latest nephrology research, it should be the last resort. One of the most severe side effects of Kayexalate is gastrointestinal tract ulceration and/or necrosis which can lead to perforation and further complications.

Even though hyperkalemia is benign most of the time, ED physicians should be vigilant and on the lookout for it in ESRD patients. When symptomatic, aggressive measure should be taken and nephrology should be consulted immediately.

Senior Report 6.24

Case Presentation by Dr. Stefanie Wise

53-year-old man presents to the ED complaining of dizziness. His symptoms started approximately 30 minutes prior to arrival. He had some mild abdominal pain initially, which felt like “one of my gallbladder attacks”, although it was located in the epigastric and left upper abdominal regions. The pain has improved, but his dizziness persists. He describes it as feeling lightheaded and like he is going to pass out. The room is not spinning. He has no headache, no vision loss and no hearing loss or tinnitus. He denies any focal weakness or numbness. Upon arrival his triage blood pressure is 68/34 with a heart rate of 60 and he is triaged as a medical code. Review of systems is otherwise negative.

PMH: Bicuspid aortic valve, Factor V Leiden, no previous surgeries

Medications: Warfarin, aspirin 81mg, vitamin B12

Allergies: NKDA

FH: No heart disease, no diabetes

SH: No tobacco, illicit drugs or alcohol

Physical Exam:

Vitals: Resuscitation BP 112/66, HR 86, RR 16, temp 37.6 rectal, pulse ox 100% on room air

General: Well-developed slender Caucasian man laying on stretcher, appears pale and mildly diaphoretic, calm and cooperative

Eyes: Sclera anicteric, PERRL at 3mm, EOMI

HENT: Mucous membranes moist, no intraoral lesions; trachea midline, no thyromegaly, no lymphadenopathy

CV:  Regular rhythm, intermittently bradycardic; S1 and S2 heard, no significant murmur appreciated; no JVD; pulses 2+ in all four extremities, no significant delay in capillary refill

Respiratory: Breath sounds equal and clear to auscultation bilaterally, no wheezes or crackles, no tachypnea

Abdomen: Soft, non-tender, non-distended, normally active bowel sounds; no rebound or guarding, no Murphy’s sign

Rectal: Guaiac negative brown stool

Skin: Pallor improved with Trendelenberg positioning; warm, mildly diaphoretic on arrival, no rashes, no petechiae

MSK: Normal tone, full range of motion in all extremities

Neuro: AOx3; speech is clear, face symmetrical, gait steady; strength 5/5 in all four extremities, sensation intact to light touch throughout extremities and face

Medical Course:

The patient is immediately placed on cardiac and pulse oximetry monitoring. IV is established and labs are drawn by nursing staff. IV fluid boluses are initiated.

A 12-lead ECG is performed:

6.24-1 ecg

Orthostatic vitals signs are then obtained. This is not tolerated well due to extreme positivity (50/30 standing). Bedside abdominal ultrasound is performed. There is no free fluid identified. Aorta is normal in caliber. There is no pericardial effusion. The patient is moved to the module pending laboratory studies.

Labs:

6.24-3j

6.24-2J

In the medical module, the patient experiences intermittent episodes of dizziness despite Trendelenberg positioning. During these episodes, his heart rate drops to the 40s, blood pressure approximately 60/40. Atropine 0.5mg is given , increasing his heart rate to the 50s. The decision is made to place a central line and repeat the CBC. MICU is consulted.

During the placement of the central line, the patient experiences tenesmus and passes loose, dark brown stool. Hemoccult is repeated and is again negative.

The patient begins to experience increasing generalized abdominal pain. Bedside ultrasound is repeated, demonstrating blood in Morrison’s pouch and behind the bladder. The patient has developed generalized abdominal guarding and rebound tenderness.

Repeat CBC (2 hours later):

6.24-4j

Blood products are ordered by massive transfusion protocol. General surgery is consulted. The patient is moved to resuscitation as RBCs and plasma are manually pumped. He is taken to the CT scan accompanied by the surgery senior resident and then immediately to the operating room.

6.24-5

Questions:

1) Which is true of non-traumatic splenic rupture?

a. Most cases occur in the absence of identifiable hematologic, vascular or splenic pathology

b. Malaria is the most common infectious etiology in the United States

c. Associated radiation of pain to the left shoulder is known as Kehr’s sign

d. Chronically enlarged spleens are most susceptible to rupture versus acute splenomegaly

2) Which is true of infectious etiologies of splenomegaly?

a. The majority of splenic ruptures associated with malaria occur during the acute infection with the primary attack

b. 15% of mononucleosis infection cases will have associated splenomegaly

c. Significant trauma, such as that experienced in contact sports, is required to incite spontaneous rupture

d. Surgical intervention is mandatory in cases of splenic hematoma or small tears when associated with an infectious etiology

3) Splenic artery aneurysms:

a. Are most commonly seen in middle-aged males

b. Are mostly associated with symptoms of left upper quadrant or epigastric pain

c. Carry a 70% mortality rate if rupture occurs during pregnancy

d. Are typically larger than 2 cm in diameter

 

Answers

1. C

Non-traumatic splenic rupture is rare but life-threatening. The majority of cases occur in the presence of identifiable pathology, such as hematologic malignancy, infection, infiltration (amyloidosis) or connective tissue diseases. Worldwide, malaria is the most common cause. In the US, mononucleosis is most common. Chronically enlarged spleens are less likely to rupture than acute cases. In the event of rupture, symptoms may include vague LUQ or epigastric abdominal pain, pain radiating to the left shoulder (Kehr’s sign), tachycardia, abdominal pain with peritonitis, lightheadedness, hypotension and potentially other signs of hemorrhagic shock.

 2. A

Malaria-related splenic rupture is most common in the acute and primary infection. In mononucleosis, 50% of patients will have splenomegaly. In either infection, small inciting events such as coughing or vomiting can cause significant rupture. Although cases of large rupture with hemodynamic instability must be surgically managed, smaller tears and hematomas may be managed conservatively with observation.

3. C

Splenic artery aneurysms are most commonly associated with pregnancy, due to the increased AV shunting to the splenic vasculature. Most cases are asymptomatic, and symptoms (LUQ or epigastric abdominal pain) indicate need for intervention. The majority of splenic aneurysms are less than 2 cm in size, making diagnosis by physical exam difficult. Diagnosis is most often incidental by ultrasound or CT, with confirmation by angiogram. While only 2% of splenic artery aneurysms lead to life-threatening rupture, 95% of the ruptures occur in young pregnant women, carrying a 70% mortality rate if they do rupture during the pregnancy.

Case conclusion: The patient was taken to the operating room for splenectomy. Pathology revealed wall rupture of an intra-splenic artery and associated hematoma without any other identifiable abnormality. The patient required no further post-surgical transfusion of blood products. He improved quickly and on post-operative day #3 was transferred to his primary health care team’s hospital for evaluation and further management of possible acute versus chronic endocarditis of his aortic valve.

Sources

– Becker, J. et al. (2006) Essentials of Surgery. Philadelphia: Saunders Elsevier.

– Gedik, E. et al.  Non-traumatic splenic rupture: Report of seven cases and review of the literature. World J Gastroenterol (2008) 14(43): 6711-6716)

– Marx, J. et al. (2010) Rosen’s Emergency Medicine 7th edition, Volume 1. Philadelphia:   Mosby Elsevier.