Page 110 - JSOM Summer 2023

hemodynamically stable and afebrile, with pulse oximetry “cross-overs” more comfortable for the swimmer but has po-
reading in the high 90s to 100%. Physical exam was nota- tentially deadly complications. The most well-known compli-
ble for generalized weakness without focal neurologic deficit, cation of this practice is known as shallow water (hypoxic)
Trousseau’s sign immediately upon application of the blood blackout. Shallow water (hypoxic) blackout is syncope due to
pressure cuff, and Chvostek’s sign. Electrocardiogram was no- cerebral hypoxia that occurs underwater while breath-holding.
table for a minimally prolonged corrected QT interval (QTc) The swimmer is much more susceptible to syncope due to hy-
of 452msec (Figure 1). poxia after blunting their hypercapnic respiratory drive. 7–9

Chest x-ray was without evidence of pulmonary edema (Fig- In the presented case, the patient admitted to hyperventilation
ure 2). between “cross-overs,” but instead of experiencing shallow
water (hypoxic) blackout, acute respiratory alkalosis ensued.
Acute respiratory alkalosis causes an increase of the pH, in-
creasing the glycolytic activity of phosphofructokinase. This
causes intracellular shifting of phosphate and intravascular/
6
FIGURE 1 Patient’s extracellular phosphate depletion. This redistribution of
EKG upon arrival phosphate was most likely the mechanism for this patient’s
to the Emergency hypophosphatemia, causing altered mental status, general-
Department. ized weakness, and potentially respiratory distress from di-
aphragmatic weakness. His hypophosphatemia was likely
exacerbated by a prolonged training day causing ATP deple-
tion, leading to further intracellular shunting of phosphate
for glycolysis. After just 20 minutes of hyperventilation at an
end-tidal carbon dioxide range of 15 to 20mmHg, phosphate
may drop below 1.00mg/dL and can take up to 90 minutes to
return to baseline. 6

FIGURE 2 Patient’s Chest Additionally, the patient’s presentation demonstrated classic
X-Ray upon arrival to the stigmata of hypocalcemia due to acute respiratory alkalosis.
Emergency Department. Acute respiratory alkalosis leads to an increase in the pH of
the serum, which causes hydrogen ion dissociation from serum
protein. Ionized calcium then drops as the unbound serum pro-
teins bind up serum calcium. 10,11 This transient hypocalcemia
was likely the cause of the patient’s tetany, prolonged QTc,
Chvostek’s sign, and Trousseau’s sign. His initial episode of
Laboratory analysis was most notable for a critically low right arm cramping was likely a variation of Trousseau’s sign
phosphate level of 1.00mg/dL (normal: 2.5–4.5mg/dL). Addi- as his right arm hung on the gunwale causing compression
tional laboratory abnormalities included low ionized calcium to the surrounding tissues. Other concerning complications
at 1.15mmol/L (normal, 1.2–1.42mmol/L), creatine kinase of of acute hypocalcemia include laryngospasm, bronchospasm,
875U/L (normal, 29–308U/L), and mild transaminitis. The pa- hypotension, cardiomyopathy, heart failure, atrioventricular
tient was initiated on 1L of intravenous Lactated Ringers and block, seizure, and coma. 12
was coached to slow his breathing. After a short period, his
respiratory distress abated, and his physical exam normalized. Aside from acute respiratory alkalosis, there are a myriad of
The patient was treated with oral phosphate repletion after other conditions that may cause hypocalcemia. Many of these
repeat phosphate level was drawn, but just prior to the lab re- conditions are genetically and parathyroid hormone medi-
sulting. The patient’s phosphate had normalized to 2.6mg/dL ated. The most well-known of these include familial isolated
even prior to supplemental phosphate treatment. The patient hypoparathyroidism, DiGeorge syndrome, Wilson’s disease,
did not have myoglobinuria, and his creatine kinase was not and hemochromatosis. Acquired causes of hypocalcemia in-
considered five times the upper limit of normal, so he was dis- clude vitamin D deficiency, malabsorption, chronic kidney dis-
charged with strict return precautions for rhabdomyolysis. On ease, “Hungry bone” syndrome, end-stage liver disease, acute
follow-up, the patient continued to be asymptomatic and had pancreatitis, post-surgical hypoparathyroidism, hypo/hyper-
no subsequent complications from this episode. magnesemia, radiation, and sclerotic metastases. A myriad
of drugs, including loop diuretics, phosphate, foscarnet, an-
ti-epileptics, magnesium sulfate, calcitonin, bisphosphonates,
Discussion
denosumab, Ethylenediaminetetraacetic acid (EDTA), and ci-
“Cross-overs” entail subsurface swimming a pool length nacalcet, may also cause hypocalcemia. Finally, and most rel-
followed by a “hand-over-hand” return along the gunwale, evant to military medicine, citrate within blood products may
maintaining their face above the water to be monitored by cause acute hypocalcemia upon transfusion, further contribut-
instructors. This is performed at a minimum recovery-to-work ing to acidosis, coagulopathy, and hypothermia in the injured
ratio of 2:1. Although they are frequently instructed not to, trauma patient. 13,14
swimmers may intentionally hyperventilate to decrease their
hypercapnic respiratory drive during the subsurface portion Another more commonly observed pool injury for the Com-
of the “cross-over.” Decreasing the hypercapnic respiratory bat Swimmer is swimming-induced pulmonary edema (SIPE).
drive, which is stimulated by carbon dioxide levels within When the patient was initially in respiratory distress, the DMT
the chemoreceptors of the medulla oblongata, makes the who pulled him out of the water was most concerned about

108 | JSOM Volume 23, Edition 2 / Summer 2023