Intraoperative Hemorrhage

History. Four hours after abdominal surgery for a splenic sarcoma, a 30-kg, 9-year-old male Labrador retriever is observed to be severely lethargic and recumbent. An abnormally large amount of blood had been lost during the surgical removal of the spleen because the dog had a hereditary blood-clotting defect (von Willebrand’s disease).

Clinical Examination. The dog’s gums are pale, and his capillary refilling time is abnormally prolonged (3 seconds). His extremities are cool to the touch. The femoral pulse is rapid and weak. An electrocardiogram indicates sinus tachy­cardia at a rate of 185 beats/min. The hematocrit (packed cell volume) is 38%, and the plasma protein concentration is 5.6 g/dL; both these values are below normal. A jugular catheter is inserted, and central venous pressure is measured and found to be -1 mm Hg (normal, O to +3 mm Hg). Despite the intra­venous administration of 600 mL Oflactated Ringer’s solution during surgery, the dog has not produced any urine. About IOOmL of blood-tinged fluid is removed from the abdomen by abdominocentesis.

Comment. This case illustrates the clinical signs that are typical of hemorrhage. Most of the blood in a dog is in the systemic veins, so most of the blood missing after hemorrhage is missing from the veins. The result is an abnormally low central venous pressure, as observed in this dog. The decreased central venous pressure causes a decreased ventricular preload and a decreased ventricular end-diastolic volume. This leads to decreases in stroke volume (Starling’s law of the heart), cardiac output, and arterial blood pressure. Inadequate cardiac output and blood pressure lead to behavioral depression.

Neiirohiimoral compensation for the hemorrhage is initiated by the atrial volume receptor reflex and the arterial baroreceptor reflex. Heart rate is increased by the combination of increased sympathetic activation and decreased parasympathetic activa­tion.

Hemorrhage per se does not reduce either the hematocrit or the plasma protein concentration, because whole blood is being lost. However, two factors caused the hematocrit and plasma protein concentration to decrease in this dog. First, the fluid administered intravenously during surgery (lactated Ringer’s) contained neither red blood cells nor plasma proteins, so the cellsand proteins remaining in the bloodstream were diluted by the addition of the fluid. Second, the hemorrhage reduced not only venous and arterial pressures but also capillary hydrostatic pressure, which changed the balance of hydrostatic and oncotic forces (“Starling forces”) across the capillary walls in favor of reabsorption. The interstitial fluid that was reabsorbed into the bloodstream contained no red blood cells and almost no plasma proteins. This caused a further dilution of the cells and proteins in the blood.

Treatment. Therapy for this dog involves measures to stop ongoing blood loss and to restore the lost blood volume. In this dog the hemorrhage is predominantly seepage from small intraabdominal vessels as a result of the coagulation defect. Transfusions of fresh blood or plasma, or concentrated prep­arations of clotting proteins, would promote clotting, limit sub­sequent hemorrhage, and expand the intravascular fluid vol­ume. Additional crystalloid solutions (e.g., lactated Ringers) also can be infused into this dog because the hematocrit and plasma protein concentration are not dangerously low. If crys­talloid solutions are administered, the hematocrit and plasma protein concentration should be monitored closely to avoid the hypoxia that results from too much dilution of the red blood cells, or the edema that results from too much dilution of the plasma proteins. Renal function should be monitored closely because the combination of hypoxia and reflex vasoconstriction can lead to ischemic damage, resulting in renal failure.