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American Journal of Emergency Medicine (2013) 31, 444.e1–444.e3

Case Report

Profound alkalemia secondary to gastric outletobstruction and acute renal insufficiency

Abstract

Alkalemia in patients presenting to the emergencydepartment can be from a multitude of causes. Althoughmost individuals will present with relatively mild tomoderate alkalemia (pH b7.65) that is readily correctable,severe life-threatening alkalemia can occur. Prompt recog-nition of the etiology of profound alkalemia and aggressiveintervention may lead to successful outcomes in patientswith pH levels that are generally considered incompatiblewith life. A 54-year-old man with a complicated surgicalhistory resulting in gastric outlet obstruction requiringcontinuous gastrotomy tube drainage presented withrecurrent syncopal episodes, a generalized tonic-clonicseizure, fluctuating mental status, and persistent tachypnea.Laboratory studies showed new-onset renal failure (bloodurea nitrogen, 87 mg/dL; creatinine, 4.2 mg/dL), severehypophosphatemia (phosphorous, 0.5 mg/dL), and anarterial pH of 7.89. The patient was aggressively fluidresuscitated, treated with carbonic anhydrase inhibitordiuretics (acetazolamide), and had potassium replacement,and a normalization of the pH occurred within 36 hours.This patient presents with one of the highest pH levelsrecorded in a patient who ultimately survived. The etiologyof this profound alkalemia was a result of both renal andgastrointestinal causes. Although hydrochloric acid in-fusions and hemodialysis with low bicarbonate dialysissolutions have been advocated by some experts in cases ofprofound alkalemia, this patient responded rapidly to moreconservative measures including intravenous hydration anddiuresis with carbonic anhydrase inhibitors.

Metabolic alkalosis is the most frequently encounteredacid-base abnormality in the hospital setting [1]. Althoughtypically mild, severe life-threatening alkalemia can occur.Death becomes increasingly likely as pH levels rise, withhistorical data describing mortality rates of 80% with pHlevels exceeding 7.65 [2]. Prompt recognition and initiationof treatment are imperative in the prevention of death in this

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high-risk population. We report a case of profoundsymptomatic alkalemia in an individual surviving one ofthe highest pH levels (pH of 7.89) ever reported.

A 54-year-old man presented with a 3-day history ofincreased confusion, multiple syncopal episodes, and ageneralized tonic-clonic seizure that occurred shortly beforeemergency department presentation. His medical history wassignificant for a perforated peptic ulcer 2 months previouslywith a complicated postoperative course resulting in gastricoutlet syndrome requiring jejunostomy tube feeds and adraining gastrotomy tube.

The patient presented in moderate respiratory distresswith a rate of 36 breaths per minute, temperature of 37.8°C,blood pressure of 139/102 mm Hg, pulse rate of 112 beatsper minute, and pulse oximetry of 99% on 2 L/min nasalcannula. He was arousable to mild physical stimulation withorientation to person only. Pulmonary examination demon-strated tachypnea with clear lung sounds. Cardiovascularexamination revealed tachycardia with no abnormal heartsounds. Abdomen was diffusely tender with a draininggastrotomy tube filled with clearish yellow nonbiliarycolored fluids. Extremities were dry, diffusely hyperreflexicwith intermittant myoclonic-type jerking and carpopedalspasms noted.

Initial laboratory studies demonstrated a sodium of 147mEq/L; potassium, 3.6 mEq/L; chloride, 94 mEq/L;bicarbonate, 34.6 mmmol/L; blood urea nitrogen (BUN),87 mg/dL; and creatinine 4.2 mg/dL. Arterial blood gasrevealed a pH of 7.89 with a PCO2 of 17, a PO2 of 80 mm Hg,and O2 saturation of 98.9%. Other studies included an ionizedcalcium of 1.02 mmmol/L; magnesium, 1.5 mEq/L; lactate,3.3 mmol/L; phosphorous, 0.5 mg/dL; and a repeat venouspH reported as an identical 7.89.

The patient was aggressively hydrated with 4 L of 0.9normal saline through peripheral and then central venousaccess over the initial 2.5 hours. Potassium phosphorousand acetazolamide were administered intravenously withimprovement noted in clinical status and laboratorymarkers. At 36 hours from the time of initial hospitaliza-tion, the patients had near normalization of the alkalemia(pH 7.46; PCO2, 38 mm Hg; HCl−, 24 mEq/L) andimproved renal function (BUN, 23 mg/dL, and creatinine,

444.e2 Case Report

1.6 mg/dL). The patient was discharged from the hospital4 days after initial presentation upon return to hisbaseline status.

Metabolic alkalosis is a primary pathophysiologicprocess resulting from either a loss of extracellular acidsor the gain of bicarbonate producing an elevated serumbicarbonate level and extracellular pH. Severe metabolicalkalosis typically involves abnormalities of either thegastrointestinal or renal system. Common gastrointestinalsources include persistent vomiting of hydrochloric acid-richgastric secretions and ingestion of exogenous bicarbonate(milk-alkali syndrome). Clinical states involving the kidneyresponsible for alkalosis are multiple including, amongothers, Cushing syndrome, hyperaldosteronism, licoriceingestion, and diuretic effects as well as Bartter andGitelman syndromes [3].

In the kidney, reabsorption of bicarbonate occurs in theproximal tubules, whereas acid secretion occurs in the distalrenal tubule via adenosine triphosphatase pumps, simplemembrane diffusion, and concentration-driven antiporters. Inthe dehydrated patient, this pathway becomes shifted towardincreasing bicarbonate retention. The renal system can thenbe both solely responsible for alkalosis as well as furtherperpetuating alkalosis produced from gastrointestinal fluidlosses [4].

Hypochloremic alkalosis is not an infrequent finding inindividuals with gastric outlet obstructions. Of the 3 highestpH levels (pH 7.87-7.95) we were able to identify in adults inthe English-language literature, all were found amongindividuals with gastric outlet obstruction as the underlyingetiology [5-7]. Although excessive loss of gastric hydro-chloric acid secretions in our case was undoubtedlyresponsible for the initial alkalemia, numerous other factorsappeared to play a role in the dramatic pH elevation as well.Hypovolemia secondary to profound vomiting results in adecreased glomerular filtration rate with bicarbonate unableto be filtered through the renal tubules. An additionaldecrease in the glomerular filtration rate occurs because ofdecreased potassium as well as increased rennin andaldosterone secretion because of dehydration. Bicarbonatethat is filtered into the renal tubules may be reabsorbedsecondary to volume contraction. A final insult to the acid-base status occurs in the setting of hypokalemia via the H-K-adenosine triphosphatase pump as the kidneys preferentiallymaintains the body's potassium levels at the expense ofacidification of the urine [3].

Table Laboratory studies associated with the 4 highest pH levels rep

pH PO2(mm Hg)

PCO(mm

Tugrul et al [5] 7.87 (venous) 34 23.Garry et al [6] 7.95 (arterial) 124 17.Gardner and Fournier [7] 7.92 (arterial) 55 23Betten et al 7.89 (arterial) 80 17

With progressive alkalemia, multiorgan dysfunctionensues. Cerebral blood flow is decreased with confusionand lethargy that may progress to seizures and coma ifuntreated. Paresthesias, muscle spasm, myoclonus, andtetany are commonly reported. Myocardial dysfunctionoccurs because of decreased inotropic effects, coronaryartery vasoconstriction, and electrolyte-mediated arrhythmia[1,8]. Coinciding electrocardiographic changes include Q-Tprolongation and U waves that are seen with the hypocalce-mia, hypomagnesemia, and hypokalemia frequently found inthe setting of alkalemia.

A centrally occurring compensatory hypoventilation isreported in many individuals with mild to moderate alkalosiswith PCO2 levels rising up to 60 mm Hg; however, this wasnot seen in our patient [9]. In fact, our case found similarfindings to those other reported cases involving extremealkalosis in which all individuals had a contributingrespiratory alkalosis [4-6] (Table). With this protectivehypoventilatory compensatory lost, the respiratory alkalosisdrives the pH further upward, worsening the acid-base state.Because of the profoundly elevated pH levels, there may bealteration in cellular oxygen delivery due to strongerhemoglobin-oxygen affinity and vasoconstriction in additionto alterations in the redox potential of cytochrome ccontributing to further end-organ toxicity.

The mainstay of therapy should focus on addressinghypovolemia and ensuring adequate urine production viaaggressive fluid resuscitation. Electrolyte replacement isparamount, with a specific emphasis on replacing potassiumto avoid persistent bicarbonate reuptake in the distal renaltubules. The use of potassium-sparing carbonic anhydraseinhibitors such as acetazolamide should be stronglyconsidered to decrease urinary bicarbonate excretion. Theuse of a hydrochloric acid infusions has been advocated bysome authors to more rapidly reverse alkalemia; however,this intervention was not found to be necessary in our caseas with aggressive fluid hydration and acetazolamide aloneour pH were normalized [10]. Other proposed interventionsinclude the use of an acid solution diasylate media as wellas intubation with allowance for hypercapnea and respira-tory acidosis to rapidly reduce elevated pH level [11,12].Despite these more aggressive treatment regiments, rapidreduction in the degree of alkalemia was found to beachieved in this and several other cases of severe alkalemiawith aggressive hydration and carbonic anhydrase inhibitorsalone [4-6].

orted in the English-language literature

2

Hg)HCO3

−

(mmol/L)Chloride(mEq/L)

BUN Creatinine(mg/dL)

7 48.2 72 10.6 1.02 44.5 62 17.9 1.6

48 40 60 4.234.6 94 87 4.2

444.e3Case Report

David P. Betten MDDepartment of Emergency Medicine

Michigan State University College of Human MedicineSparrow Health System, Lansing, Michigan, USA

E-mail address: bettend@msu.edu

Daniel J. Bridger DOSection of Emergency Medicine

Department of Internal MedicineMichigan State University College of Osteopathic Medicine

Sparrow Health System, Lansing, Michigan, USA

Brent M. Felton DOSection of Emergency Medicine

Department of Internal MedicineMichigan State University College of Osteopathic Medicine

McClaren Regional Medical CenterLansing, Michigan, USA

http://dx.doi.org/10.1016/j.ajem.2012.05.025

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[6] Garry P, Tormey WP, Harte M. Arterial blood pH of 7.95 in an adultwith pyloric stenosis. Clin Chem 1993;39:1554-5.

[7] Gardner LB, Fournier AM. Extraordinary alkalemia and triple acid-base disturbance. South Med J 1984;77:265-8.

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[9] Lavie CJ, Crocker Jr EF, Key KJ, Ferguson TG. Marked hypo-chloremic metabolic alkalosis with severe compensatory hypoventila-tion. South Med J 1986;79:1296-9.

[10] Kwun K, Boucherit T, Wong J, et al. Treatment of metabolic alkalosiswith intravenous infusion of concentrated hydrochloric acid. Am JSurg 1983;146:328-30.

[11] Blank MG, Lew SQ. Hypoventilation in a dialysis patient with severemetabolic alkalosis: treatment by hemodialysis. Blood Purif 1991;9:109-13.

[12] Ayus JC, Olivero JJ, Adrogue HJ. Alkalemia associated with renalfailure—correction by hemodialysis with low-bicarbonate dialysate.Arch Intern Med 1980;140:513-5.