Page 70 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
P. 70

60         ELECTROLYTE DISORDERS


            vomiting, ataxia, diarrhea, and tremors. These ingredients  patients with underlying cardiac disease. Patients with
            act as osmotic laxatives, causing a shift in water from the  CDIorNDItypicallyarepresentedforevaluationofsevere
            tissues into the lumen of the bowel and resulting in  polydipsia and polyuria.
            hypernatremia. Warm water enemas may facilitate
            removal of paintball ingredients from the bowel, but  TREATMENT OF
            activated charcoal products generally should not be used
            because they may contain sorbitol. Depending on the  HYPERNATREMIA
            duration of onset, 5% dextrose in water (acute onset) or
                                                                 The main goals in treating patients with hypernatremia
            0.45% NaCl (unknown onset) can be administered to
                                                                 are to replace the water and electrolytes that have been
            gradually correct hypernatremia. Parenteral fluids can
                                                                 lost and, if necessary, to facilitate renal excretion of excess
            be supplemented with potassium chloride if serum
                                                                 sodium. The first priority in treatment should be to
            potassium concentration decreases below 2.5 mEq/L.
                                                                 restore the ECF volume to normal. The next priority is
               Therapeutic administration of hyperosmolar solutions
                                                                 to diagnose and treat the underlying disease responsible
            containing large amounts of sodium during cardiac
                                                                 for the water and electrolyte deficits.
            resuscitation can cause hypernatremia and hypertonicity
            (e.g., hypertonic saline, sodium bicarbonate). For exam-  PURE WATER LOSS
            ple, serum sodium concentration reached 174 mEq/L
            within 15 minutes after beginning infusion of 7.2% NaCl  Total body solute (TBS) is the product of TBW and
                                               2
            at a rate of 15 mL/kg in normal beagles. Sodium phos-  plasma osmolality (P osm ). If a patient’s fluid loss has been
            phate enemas may also result in mild hypernatremia. 3  limited to pure water, the following relationship is true:
            Primary hyperaldosteronism also may be associated with
            hypernatremia. It is rare in dogs, but several cases                  TBS presentÞ ¼ TBS previousÞ
                                                                                      ð
                                                                                                    ð
            have been reported in cats (see Chapter 5 ). Mild       TBW presentÞ   P osm presentð  Þ ¼ TBW previousÞ
                                                                                                     ð
                                                                        ð
            hypernatremia  also  may  occur   in  dogs  with
            hyperadrenocorticism. 101,128                                                         P osm previousð  Þ
            CLINICAL SIGNS OF                                    If we assume that body water (TBW) is 60% of body
            HYPERNATREMIA                                        weight measured in kilograms (Wt) and that 2.1   P Na
                                                                 is an estimate of P osm :
            The clinical signs of hypernatremia primarily are neuro-
                                                                                                   ð
            logic and related to osmotic movement of water out of        2:1   P Na presentð  Þ   0:6   Wt presentÞ
            brain cells. A rapid decrease in brain volume may cause    ¼ 2:1   P Na previousð  Þ   0:6 Wt previousÞ
                                                                                                  ð
            rupture of cerebral vessels and focal hemorrhage. The
            severity of clinical signs is related more to the rapidity  This equation reduces to:
            of onset of hypernatremia than to the magnitude of
            hypernatremia. In dogs and cats, clinical signs of              P Na presentð  Þ   Wt presentÞ ¼
                                                                                            ð
            hypernatremia are observed when the serum sodium                P Na previousð  Þ   Wt previousÞ
                                                                                             ð
            concentration  exceeds  170  mEq/L. 66,78,84,133  If
            hypernatremia develops slowly, the brain has time to adapt              P Na ðpresentÞ  WtðpresentÞ
            to the hypertonic state by production of intracellular    WtðpreviousÞ¼
                                                                                          P Na ðpreviousÞ
            solutes (e.g., inositol and amino acids) called osmolytes
            or idiogenic osmoles. These substances prevent dehy-
                                                                 The water deficit is the difference between the previous
            dration of the brain and allow patients with chronic
                                                                 and present body weights:
            hypernatremia to be relatively asymptomatic.
               Where described in dogs and cats, clinical signs of
                                                                                 Wt previousÞ   Wt presentÞ ¼
                                                                                   ð
                                                                                                 ð
            hypernatremia and hypertonicity have included anorexia,
            lethargy, vomiting, muscular  weakness, behavioral         P Na ðpresentÞ  WtðpresentÞ    WtðpresentÞ
            change, disorientation, ataxia, seizures, coma, and              P Na ðpreviousÞ
            death.* If hypotonic losses are the cause of hypernatremia,
            clinical signs of volume depletion (e.g., tachycardia, weak  or
            pulses, and delayed capillary refill time) may be observed

            on physical examination. If hypernatremia has developed                     P Na ðpresentÞ
                                                                         WtðpresentÞ                  1
            as a result of a gain of sodium, signs of volume overload                  P Na ðpreviousÞ
            (e.g., pulmonary edema) may be observed, especially in
                                                                 Consider a previously normal dog that has been deprived
            *References 5, 23, 27, 31, 34, 78, 84, 133, 159.     of water for several days. The dog weighs 10 kg at
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