Page 1395 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

968 PART 8: Renal and Metabolic Disorders

cases were found among nearly 20,000 nonobstetric patients who had • Forsythe R, et al. Parenteral calcium for intensive care unit
magnesium levels checked. 298 patients. Cochrane Database Syst Rev. 2008(4).
Etiologies: The most common cause of hypermagnesemia is renal • Halperin mL, Kamel KS. Potassium. Lancet. 1998;352(9122):135-140.
insufficiency. Patients with progressive renal insufficiency maintain • Lindner G, et al. Hypernatremia in the critically ill is an indepen-
magnesium balance by increasing the fractional excretion of magnesium dent risk factor for mortality. Am J Kidney Dis. 2007;50(6):952-957.
(FeMg). Patients with severe renal insufficiency have an FeMg of nearly
100%, which allows preservation of magnesium balance despite severe • Ralston SH, et al. Comparison of three intravenous bisphosphonates
decreases in GFR. 299 in cancer-associated hypercalcaemia. Lancet. 1989;2(8673):1180-1182.
Symptomatic hypermagnesemia (despite normal renal function) has • Schrier RW, et al. Tolvaptan, a selective oral vasopressin V2-receptor
been reported with magnesium infusions. The typical setting is the antagonist, for hyponatremia. N Engl J Med. 2006;355(20):2099-2112.
treatment of preterm labor or preeclampsia/eclampsia. Standard obstet- • Stewart AF. Clinical practice. Hypercalcemia associated with
ric protocols (4- to 6-g load followed by 1 to 2 g/h) result in serum mag- cancer. N Engl J Med. 2005;352(4):373-379.
nesium levels of 4 to 8 mg/dL. Patients suffering accidental parenteral
300
magnesium overdoses usually have good outcomes, despite significant • Wahr JA, et al. Preoperative serum potassium levels and periop-
short-term morbidity and magnesium levels as high as 24 mg/dL. 301,302 erative outcomes in cardiac surgery patients. Multicenter Study
Sequelae in the newborn have been linked with magnesium administra- of Perioperative Ischemia Research Group. JAMA. 1999;281(23):
tion in a dose-dependent fashion and include hypotonia, osteopenia, 2203-2210.
and increased rates of admission to neonatal intensive care units. 303-305
Hypermagnesemia due to ingestion of magnesium is unusual in the Acknowledgment: The authors wish to thank the previous edition
absence of renal insufficiency. In one retrospective study of hypermagne- chapter authors Joel Michels Topf and Steve Rankin for their work
semia, excluding obstetric admissions all cases were due to oral intake and on the previous chapters, portions of which form the basis for this
the average creatinine was 4.8. Oral sources of magnesium include antac- current chapter.
ids and Epsom salts. 306-308 Chronic oral ingestions of magnesium result in
severe symptoms, including death. Hypermagnesemia has been repeatedly REFERENCES
reported following the use of magnesium-containing enemas. 309-312
Complete references available online at www.mhprofessional.com/hall
Clinical Sequelae: Magnesium can block synaptic transmission of nerve
impulses. Hypermagnesemia causes loss of deep tendon reflexes, and may
lead to flaccid paralysis and apnea. 298,301,313,314 Neuromuscular toxicity also
affects smooth muscle, resulting in ileus and urinary retention. In cases
315
of oral intoxication, the development of ileus can slow intestinal transit CHAPTER Acid-Base Balance
times, increasing absorption of magnesium. Hypermagnesemia has also
306
been reported to cause parasympathetic blockade, resulting in fixed and 100 David C. Kaufman
dilated pupils, mimicking brain stem herniation. Other neurologic signs Andrew J. Kitching
301
include lethargy, confusion, and coma 298,301,314 (see Table 99-17). John A. Kellum
Cardiovascular manifestations of hypermagnesemia initially include
bradycardia and hypotension. 298,306,314 Higher magnesium levels cause
PR interval prolongation, increased QRS duration, and prolonged QT KEY POINTS
interval. Extreme cases can result in complete heart block or cardiac • The blood [H ] and pH are determined by the strong ion differ-
298
+
arrest. One case of ventricular fibrillation has been reported with an , and the total concentration of weak acids,
Mg level of 9.7 mg/dL. 302 ence (SID), the P CO 2
2+
mostly consisting of phosphate and albumin.
Treatment: The first principle of treatment is prevention. Patients with • Both acidemia and alkalemia have potentially harmful physiologic
renal insufficiency should not be given magnesium-containing antacids effects, and the presence of either is related to mortality.
or cathartics. In cases of hypermagnesemia, stopping the infusion or • Most acid-base derangements do not benefit from specific correc-
supply of magnesium will allow patients with intact renal function to tion of the abnormal pH; instead, the intensivist should focus on
recover. Initiation of IV fluids and loop diuretic should also be con- detecting and treating the underlying condition.
sidered, particularly in those with mild to moderate renal impairment.
Calcium salts can reverse hypotension and respiratory depression. • Acid-base disorders are easily characterized using a stepwise approach.
316
Patients are typically given 100 to 200 mg of elemental calcium intrave- • Lactic acidosis is the most important acid-base abnormality in
nously over 5 to 10 minutes. ICU patients. Inadequate tissue oxygenation underlies the lactic
In patients with severe renal dysfunction, dialysis offers a way to acidosis in some patients (acute hemorrhage, critical hypoxemia,
rapidly clear magnesium. Though both peritoneal and hemodialysis can cardiogenic shock) but probably does not in others (such as the
lower magnesium in an acute situation, hemodialysis is the preferred resuscitated septic patient).
modality. 298,306,317 Continuous renal replacement therapy is also effective
at lowering serum magnesium, but is slower than hemodialysis. 314

Acid-base balance and acid-base disorders are imperfect terms for the
KEY REFERENCES determining factors and disease processes that lead to a particular
hydrogen ion concentration [H ] in the blood. The methodology used
+
• Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000; routinely to determine an acid-base disorder is accurate in defining the
342(20):1493-1499. disturbance. This methodology does not, however, isolate the variables
• Adrogue HJ, Madias NE. Hyponatremia. N Engl J Med. 2000; that have led to a particular [H ] in blood. The components of blood
+
342(21):1581-1589. that contribute to acid-base balance are
• Danziger J, et al. Proton-pump inhibitor use is associated with low 1. Water
serum magnesium concentrations. Kidney Int. 2013;83(4):692-699.
2. Strong cations (Na , Mg , Ca , K ) and strong anions (Cl , lactate )
+
−
−
2+
+
2+

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