Intern Report 8.17

internreport

Case Presented by Jeff Butler, MD

Chief Complaint: abdominal pain, diarrhea, weakness

HPI: An otherwise healthy 6yo boy presents with three days of abdominal pain, nausea, vomiting, and diarrhea. His symptoms started with nausea and vomiting, and were followed by fever and epigastric, cramping abdominal pain. By Day 2 of his illness he was having frequent loose stools up to 15 times per day. The mother decided to bring the child in after he developed some weakness and difficulty walking prior to arrival. The vomiting occurred around 2-4 times per day and was characterized as nonbloody and nonbilious. There was also no blood noted in the stool. The child has had a poor appetite in the last two days and has been refusing meals after two episodes of post-prandial emesis. The mother thinks the child may have been urinating less frequently since this morning. The fever is being treated with alternating motrin and Tylenol last given 2 hours prior to arrival. The child had multiple sick contacts with similar symptoms at daycare and there was no history of recent travel.

ROS:
Constitution: positive for fevers, negative for weight change
HEENT: negative for ear pain, sore throat
Cardiac: negative for chest pain, palpitations
Pulm: negative for wheezing, cough
GI: positive for abd pain, diarrhea, vomiting
GU: positive for decreased urination
MSK: negative for joint pain, swelling, myalgia, positive for weakness
Neuro: positive for dizziness, HA

PMHX: none

PSHx: none

Allergies: NKDA

Meds: Motrin, Tylenol PRN fever

SocHx: no tobacco use in the home, patient attends school and daycare, lives with mom, dad, two brothers.

PE:
Vitals: T37.1, HR140, BP100/60, R20, SpO2 99% RA
General: Ill-appearing male child sitting on the exam table in mild distress due to weakness
Eyes: PERRL, EOM, no pallor
HENT: Normal tympanic membrane without erythema or purulent drainage, dry oral mucous membranes, neck supple and nontender without LAD
CV: Tachycardic regular rate with normal hearts sounds, pulses 2+ at radial and dorsalis pedis bilaterally, cap refill 2 seconds
Pulm: Normal work of breathing with clear breath sounds bilaterally
Abd: Soft, mildly tender to palpation over epigastrium, no rebound tenderness or guarding, normoactive bowel sounds
Skin: No rashes, bruises, or petechiae
Neuro: Normal mentation, no facial droop, tongue midleine, smiles symmetrically, 4/5 strength with hip flexion bilaterally, 4/5 strength with leg flexion and extension bilaterally, 5/5 strength otherwise throughout, sensation intact to light touch throughout, no clonus

You begin IV hydration with a 20cc/kg bolus and start weight-based maintenance fluids. Lab tests were ordered as follows:

 Labs:
CBC
WBC- 9.4
Hgb- 13.5
Plts- 278

BMP
Na- 134
Cl- 105
K- 1.9
HCO3- 19
BUN- 20
Cr- 1.1
Glu- 89

Questions:
Q1. Which of the following is a spurious cause of hypokalemia?
A) Recent fluid administration in the IV site
B) Sample deterioration
C) Hemolysis
D) Cold storage

Q2. What EKG finding can be found with hypokalemia?
A) Peaked T waves
B) U waves
C) J waves
D) QRS prolongation

Q3. What is the best method for replacing this patient’s electrolyte abnormalities?
A) No replacement needed
B) PO potassium
C) IV potassium
D) Yes, supplement with magnesium and IV potassium

Bonus Question:
Q4. What is the most likely acid-base disorder this patient will have? Maybe make this the bonus questions but clinically not as important as the next question
A) Respiratory acidosis
B) Metabolic alkalosis
C) AG metabolic acidosis
D) NAG metabolic acidosis

 

Answers: 1. A, 2. B, 3. D, 4. D

Discussion:

There are a couple important causes of spurious hypokalemia, most of which will be due to elements outside of your control except by thinking ahead and, for example, asking nursing staff to hold IV fluids before drawing labs. If you think the hypokalemia is spurious due to white cell consumption as in the case of the high leukocytosis usually associated with sepsis or leukemia you can call the lab and try to determine whether there were delays in analysis.
However, if the hypokalemia is clinically significant such that you suspect the need for IV supplementation you may be able to quickly verify the result based on EKG findings that include flattened T waves and U waves. Peaked T waves and QRS prolongation are more typical of hyperkalemia.
For a potassium > 2.5 mmol/L it is appropriate to replete with an oral dose of 0.5 mmol/kg for kids age < 5, and 1 mmol/kg in younger kids. However, repletion of severe hypokalemia is complicated by the fact that potassium is an irritant to peripheral veins and higher IV doses result in transiently increased cardiac concentrations that can cause cardiac arrest. This patient will likely require ICU admission for potassium repletion, cardiac monitoring, and q4-6h electrolyte checks where it will be appropriate to calculate a total body potassium deficit but a dose of 0.3 mmol/kg/h can be started in the ED through a peripheral vein. Magnesium should also be supplemented because depletion often coexists with hypokalemia, low magnesium impairs renal potassium reabsorption, and patients are at higher risk for a ventricular arrhythmia as described below.
Diarrheal stool contains a relatively high potassium content and diarrhea is the main cause of hypokalemia worldwide. The stool also contains a significant amount of bicarb, the loss of which is adjusted for by the kidneys with the H+/K+ antiporter, exchanging intracellular potassium for extracellular protons. Thus, the sufficient loss of bicarbonate ionically balanced through shifts in potassium result in a non-anion gap metabolic acidosis. The low serum potassium in the setting of this regulatory mechanism by the kidneys indicates an even more profound degree of total body potassium loss that should prompt repletion. Clinically, hypokalemia is most likely to affect the heart and muscles with severe cases of hypokalemia (< 2.5 mmol/L) resulting in complete muscle paralysis, rhabdomyolysis, and torsades or ventricular fibrillation. However, hypokalemia by itself rarely causes the cardiac complications just mentioned, and instead potentiate other causes of these like hypomagnesemia.
References:
Marx, JA, Hockerberger R, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice (8th edition), Mosby 2013.

Nickson, C. Life in the Fast Lane (http://lifeinthefastlane.com/pediatric-perplexity-010/). 2010.

Welfare, W, Sasi P, English M. Challenges in managing profound hypokalmia. BMJ. 2002. Feb 2; 324(7332): 269-70.