Gastric dilation and volvulus (Proceedings)


Gastric dilation and volvulus (Proceedings)

Nov 01, 2010

Many patients present to general, emergency, and referral specialty veterinary facilities with conditions that require immediate surgical intervention. The success or failure of the subsequent surgical procedure starts when the patient is initially presented for treatment. These patients are often respiratory, metabolically, immunologically, and/or cardio-vascularly unstable. By inducing anesthesia in these patients without pre-operative evaluation and stabilization, we may be increasing their risk of adverse effects due to anesthesia. Effective pre-surgical stabilization of the emergent surgical patient is a complex process. It involves identifying what is sub-optimal in the patient. This process also involves providing the appropriate medications to improve their physical status, and carefully and thoroughly monitoring during the stabilization phase. In most instances, taking these steps will make the patient a better anesthetic candidate. A case-based discussion with focus on pre-surgical stabilization of a patient presenting with gastric dilatation-volvulus will be used to emphasize these points.

Gastric dilatation-volvulus (GDV) is a condition where the stomach becomes abnormally distended with air (dilatation) and then rotates upon its long axis (volvulus). This pathologic change in stomach conformation commonly results in a variety of life-threatening conditions. Common presenting complaints include non-productive retching, restlessness, increased salivation, abdominal distension, and weakness. Although most commonly seen in large breed dogs, GDV can occur in any breed.

Why Resuscitate Prior to Surgery

A patient that presents for gastric dilatation-volvulus is often in a state of disequilibrium. They can have changes in fluid balance, acid-base status, or electrolyte status. These alterations may manifest as abnormal blood pressure, electrical activity of the heart, or mentation. Patients that have these disturbances are at greater risk for the cardio-vascular and respiratory effects of most anesthetic agents. Anesthetics commonly decrease vascular tone, cardiac output, and/or respiratory drive in a dose-dependent manner. When this occurs, oxygen delivery to the tissues is decreased. This can lead to acid-base and electrolyte disturbance and subsequent cellular injury and death.

The physiologic response to pain can also alter a patient's equilibrium. Pain can lead to changes in blood pressure, heart rate, or respirations. Due to these effects, the patient can develop further abnormalities in acid-base status, electrolyte balance, and oxygen delivery.

The sum total of these alterations can be poor tissue perfusion and circulatory shock. The severe gastric distention causes significant increases in intra-abdominal pressure. This can lead to obstruction of the caudal vena cava and results in decreased venous return and cardiac output and decreased blood flow to the splanchnic and genitourinary viscera. The rotation of the stomach commonly leads to rupture of the short gastric and epiploic vessels, causing significant hemorrhage and further exacerbating hypovolemia.

Shock is a condition of abnormal perfusion of tissues which leads to a critical decrease in oxygen delivery (DO2) and/or an increase in tissue consumption of oxygen (VO2) and results in altered cell metabolism, cell death, and organ malfunction or failure. However, hypotension is not a sign of shock and is only observed in the later stages of shock. Shock has multiple stages. These stages are the compensatory stage, the early decompensatory stage, and the terminal decompensatory stage. In the compensatory stage, the body senses changes in blood flow and responds by vasoconstriction, increased heart rate and increased strength of heart contraction. Because of these compensatory mechanisms, blood pressure is maintained and it is possible to miss this stage. As low blood flow persists, there is reduced blood supply to the skin, skeletal muscle, gastrointestinal tract and kidneys and ischemic injury to these organs. With prolonged poor blood flow, leads to severe tissue hypoxia and multiple organ failure. This is the terminal decompensatory stage of shock and often ends in cardio-pulmonary arrest. Because the GI tract is the shock organ in the dog, bacterial and endotoxin translocation through the damaged gastrointestinal mucosal barrier into the bloodstream occurs and septicemia may ensue. This septicemia can further exacerbate the shock by inducing inflammatory cytokine release. By addressing the potential or documented shock, acid-base abnormalities, electrolyte abnormalities, and pain early in the stabilization process, damage to tissues far from the affected organ system can be minimized, presenting a patient that is less likely to have complications while receiving general anesthesia.

How to Effectively Resuscitate the GDV Patient for Emergency Surgery

When a patient first presents with suspected gastric dilatation-volvulus, the initial step in the stabilization process is identifying and correcting abnormalities in a patient's status. Identification is accomplished via primary survey examination, laboratory evaluation of venous blood gas and electrolytes, and monitoring of blood pressure/blood flow and cardiac conduction (ECG). Pre-fluid blood samples are collected for evaluation by patient-side rapid tests such as packed cell volume (PCV), total solids (TS), electrolyte, venous blood gas, lactate, and coagulation parameters. Pre-fluid blood samples are also collected for analysis of serum biochemical profile, complete blood count, and urinalysis to be performed once time permits. Pre-fluid laboratory values provide baseline data from which subsequent values are compared to and monitored. Therapy should be initiated simultaneously and directed at attempting to normalize these parameters prior to induction of anesthesia.

The mainstay of stabilization therapy for gastric dilatation-volvulus involves the provision of fluid support. Fluid therapy increases vascular volume, thereby improving perfusion. This improved perfusion often improves many of the global perfusion abnormalities that are initially noted. Bolus fluid therapy is indicated in the severely volume depleted patient (absolute or relative). In the intravascular volume depleted patient, the volume of the fluid bolus and number of fluid boluses needed are determined based on resolution of clinical signs and normalization of measured parameters. This process is called goal-directed resuscitation, where therapy is directed to pre-determined end points. The patient should be re-assessed after each bolus to determine if the bolus has been effective in resolving the volume depleted state or if additional boluses are needed. Proper monitoring of the patient receiving fluid therapy is a hands-on endeavor. Much of the information we need is gained through serial examinations. No single parameter evaluated will necessarily provide all the information required to guide fluid therapy. Physical examination parameters that should be evaluated include a patient's weight, mentation, skin turgor, pulse rate and quality, respiratory rate and effort, serial lung auscultation for rales, mucus membrane color, and capillary refill time. If an indwelling urinary catheter is in place, serial evaluation of fluid input and urine output can provide significant information regarding whether too little or too much fluid therapy is being administered. Renal chemistry parameters (BUN, creatinine) in conjunction with urine specific gravity measurement provide additional information. Venous blood gas analysis and serum lactate measurement are other patient-side laboratory parameters that can provide information regarding tissue perfusion. Just as important, blood pressure/blood flow monitoring can provide valuable information to assess the patient's response to fluid therapy and whether sufficient fluid therapy has been administered to provide for tissue perfusion.

Crystalloid fluids are the most commonly administered therapy for resuscitation. Replacement crystalloid solutions contain dissolved solutes that approximate the solute concentration found in plasma water. These solutions are indicated for the rapid replacement of intravascular volume and electrolytes as seen with shock and hemorrhage. With replacement crystalloid fluids, only 20-25% of the infused volume of fluid remains within the intravascular space 1 hour after infusion. Therefore, large volumes of replacement crystalloids need to be administered to replace intravascular volume. The commonly available replacement solutions include normal saline (0.9% NaCl), Ringer's solution (lactate or acetate), Normosol R, and Plasmalyte A. Alone, repeated crystalloid boluses of 20-30ml/kg are administered until resuscitation goals are met. However, crystalloid fluids are often administered along with colloids to augment their vascular volume expanding effect.

Colloidal fluids are high molecular weight compounds that do not readily leave the intravascular space. They exert their effect of expanding intravascular volume by holding and potentially drawing water into the vasculature. Colloid fluid solutions are indicated for the treatment of hypovolemia and sepsis, among other conditions. Colloid solutions include plasma, human serum albumin (5% and 25%), canine specific albumin concentrates, and synthetic compounds such as hetastarch, dextrans, and Oxyglobin™. Synthetic colloids are administered in boluses of 5-10 ml/kg. When used in conjunction with colloids, smaller replacement crystalloid boluses of 15-20ml/kg are used. The maximum dose of hetastarch should not exceed 20ml/kg and of Oxyglobin™ should not exceed 30ml/kg.