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Alcohols and Glycols Chapter | 49  653




  VetBooks.ir  also increase serum osmolality. Serum osmolality is
             increased within an hour of EG ingestion, increasing
             in parallel with serum EG concentrations (Dial et al.,
             1994a,b). When measured serum osmolality (by osmome-
             try) is compared to calculated serum osmolality, the differ-
             ence is referred to as the osmole or osmolal gap. Normal
             serum osmolality is 280 310 mOsm/kg, and the normal
             osmole gap is less than 10 mOsm/kg. Serum osmolality as
             high as 450 mOsm/kg and an osmole gap as high as
             150 mOsm/kg may be seen 3 h after ingestion, depending
             on the quantity of antifreeze ingested (Jacobsen et al.,
             1982b; Grauer et al., 1984). Both the gap and the measured
             osmolality may remain significantly high for approximately
             18 h after ingestion. Multiplication of the osmole gap
             by five yields an approximate serum EG concentration in  FIGURE 49.3 Calcium oxalate monohydrate crystals (polarized light)
             mg/dL (Burkhart and Kulig, 1990). Each 100 mg/dL incre-  from a dog with EG toxicosis.
             ment increase in EG concentration contributes approxi-
             mately 16 mOsm/kg H 2 O to the serum osmolality (Eder  1996; Eder et al., 1998). Dumbbell or sheaf-shaped crys-
             et al., 1998). Simultaneous or sequential increases in  tals are observed infrequently. The detection of calcium
             osmole and anion gaps are very suggestive of EG intoxica-  oxalate crystalluria, particularly the monohydrate form,
             tion. As EG is metabolized, its contribution to the osmole  provides strong supporting evidence for the diagnosis of
             gap diminishes because the accumulating negatively  EG poisoning (Fogazzi, 1996). Urinary pH consistently
             charged metabolites do not contribute to the osmole gap  decreases following EG ingestion.
             (Eder et al., 1998). Two types of instruments are used to  Another diagnostic procedure that may be helpful in
             measure osmolality: freezing point osmometers and vapor  detecting early EG intoxication is examination of the oral
             pressure osmometers. Because EG is nonvolatile (boiling  cavity, face, paws, vomitus, and urine with a Wood’s

             point, 197 C), it is detected by either the freezing point or  lamp to determine whether they appear fluorescent. Many
             vapor pressure methods. However, methanol, ethanol, and  antifreeze solutions manufactured today contain sodium
             other volatile compounds, although contributing to serum  fluorescein, a fluorescent dye that aids in the detection of
             osmolality, may go undetected if assayed by the vapor  leaks in vehicle coolant systems. The dye is excreted in
             pressure method. Most clinical laboratories use the freezing  the urine for up to 6 h following ingestion of the anti-
             point method (Kruse and Cadnapaphornchai, 1994).   freeze (Winter et al., 1990). A negative test does not elim-
             Osmolality can be measured using serum or plasma; if the  inate the possibility of EG ingestion because not all
             latter is used, heparin is the preferred anticoagulant. Other  antifreeze solutions contain the dye.
             anticoagulants, such as EDTA, can markedly increase
             osmolality and can result in spurious increases in the
             osmole gap (Kruse and Cadnapaphornchai, 1994).     Late Laboratory Abnormalities
                Dogs are isosthenuric (urine specific gravity of  With the onset of renal damage and subsequent decreased
             1.008 1.012) by 3 h following ingestion of EG due to  glomerular filtration, serum creatinine and blood urea
             osmotic diuresis and serum hyperosmolality-induced  nitrogen (BUN) concentrations increase. In the dog, these
             polydipsia (Grauer et al., 1984; Dial et al., 1994a). The  increases begin to occur between 24 and 48 h following
             urine specific gravity in cats is also decreased by 3 h after  EG ingestion. In the cat, BUN and creatinine begin to
             ingestion but may be above the isosthenuric range (Dial  increase approximately 12 h after ingestion; however,
             et al., 1994b; Fogazzi, 1996). Calcium oxalate crystalluria  because cats do not develop polydipsia, this may be in
             is a common finding and may be observed as early as 3  part due to dehydration. Serum phosphorus concentrations
             and 6 h after ingestion in the cat and dog, respectively, as  increase at this time due to decreased glomerular filtration.
             a result of oxalic acid combining with calcium (Dial  Hyperkalemia develops with the onset of oliguria and
             et al., 1994a,b). Calcium oxalate monohydrate crystals are  anuria. Serum calcium concentration is decreased in
             variably sized, clear, six-sided prisms (Fig. 49.3)(Scully  approximately half of patients (Thrall et al., 1984b;
             et al., 1979; Terlinsky et al., 1981; Jacobsen et al., 1982a;  Connally et al., 1996) and is due to the formation of insol-
             Kramer et al., 1984; Thrall et al., 1985). In animals and  uble calcium oxalate. Clinical signs of hypocalcemia are
             people poisoned with EG, the monohydrate form is   infrequently observed because acidosis results in a shift to
             observed more frequently than the dihydrate form, which  the ionized, physiologically active form of calcium. Serum
             appears as an envelope or Maltese cross (Connally et al.,  glucose concentration is increased in approximately 50%
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