Small Animal Surgical Emergencies. Группа авторов

Small Animal Surgical Emergencies

Neoplasia Urologic Bladder, ureteral, or urethral disruption^a Bladder, ureteral, or urethral obstruction^a Nonobstructive urolithiasis Infection: cystitis, pyelonephritis Neoplasia^a Ischemia Hepatobiliary Hepatic abscess^a Hepatic torsion^a Hepatitis Hepatic laceration^a Cholangiohepatitis Biliary obstruction^a Cholecystitis Gall bladder mucocele^a Cholelithiasis Biliary disruption^a Spleen Torsion^a Neoplasia^a Hematoma Laceration Infarction^a Pancreas Pancreatitis Pancreatic abscess^a Pseudocyst^a Neoplasia Peritoneum Septic peritonitis^a Uroperitoneum^a Bile peritonitis^a Inflammatory peritonitis Hemoperitoneum^a Disseminated neoplasia Mesenteric rent^a Mesenteric volvulus^a Reproductive system: Male Prostatitis, prostatic abscess^a Prostatic/periprostatic cyst^a Neoplasia Testicular torsion^a Female Pyometra^a Uterine rupture^a Neoplasia

^a Surgical conditions or those that may benefit from surgical intervention.

Systematic Approach to Initial Stabilization: Cardiovascular System

Cardiovascular abnormalities including hypovolemia and other shock states are common in patients with acute abdominal illness and pain. Rapid initial assessment of heart rate, pulse rate, pulse quality, mucus membrane color with capillary refill time, and level of mentation, followed by a thorough cardiac auscultation are all essential for initial evaluation of the cardiovascular system.

Patients with acute abdomen may be presented in hypovolemic and/or distributive shock. Hypovolemic shock occurs when there is inadequate delivery of oxygen to the tissues due to a decrease in intravascular volume or cardiac preload. Rapid activation of compensatory mechanisms, including increased sympathetic tone, and activation of the renin–angiotensin–aldosterone system function to help maintain adequate cardiac output. As these compensatory mechanisms become overwhelmed, patients will exhibit clinical signs of decompensated shock: increased heart rate, poor pulse quality, change in mucous membrane color (to pale pink, white, or gray), prolonged capillary refill time, and depressed mentation. These physical examination changes primarily result from the reduction in blood volume and the failure of compensatory mechanisms to maintain adequate circulation and oxygen delivery. Decreased blood volume and the resultant hypovolemic shock may occur as a result of acute hemorrhage, severe dehydration from protracted vomiting/diarrhea, or from fluid shifts out of the intravascular space. While hypovolemia can develop from severe dehydration, dehydration itself does not equal hypovolemia and can be corrected over 12–24 hours. Hypovolemic shock, however, should be treated aggressively and corrected quickly over minutes to hours.

Systemic infection and sterile inflammatory states may be other causes of shock in the patient with acute abdomen. Distributive shock, characterized by peripheral vasodilation and decreased systemic vascular resistance, can occur secondary to the inflammatory response present in patients with the systemic inflammatory response syndrome (SIRS). Dogs must fulfill three of the four criteria and cats two of the four criteria for the diagnosis of SIRS, which include tachycardia (or bradycardia in cats), tachypnea, and/or hyperventilation, hyperthermia or hypothermia, and the presence of a leukopenia (white blood cell count < 5000/μl), leukocytosis (white blood cell count > 18 000/μl), and/or left shift (> 5% bands) [3]. Sepsis criteria have recently been updated in human medicine, such that sepsis is defined as a life‐threatening organ dysfunction caused by dysregulated host response to infection [4]. Patients with septic shock can be identified with a clinical construct of sepsis with persistent hypotension requiring vasopressors to maintain mean arterial blood pressure 65 mmHg or higher and having a serum lactate level greater than 2 mmol/l (18 mg/dl) despite adequate volume resuscitation.

Resuscitation and Management of Cardiovascular Abnormalities

The ultimate goal of stabilizing any patient with major body system abnormalities is maximizing oxygen delivery. The total oxygen delivery depends on both cardiac output and the oxygen content of the arterial blood (CaO₂), and compromise of either will contribute to tissue hypoxia. Initial treatment for hypovolemia includes rapid intravenous fluid replacement to optimize preload and cardiac output, and initial oxygen therapy to maximize blood oxygen content. Before volume resuscitation, the patient's heart and lungs should be ausculted critically to rule out any primary cardiac abnormality that could be contributing to the shock state (cardiogenic shock). At the time of intravenous catheter placement and before fluid administration, blood samples for an emergency database should be obtained, including packed cell volume (PCV) and total solids, blood glucose concentration, blood lactate concentration, and arterial or venous blood gas with electrolytes, blood urea nitrogen (BUN), and creatinine. A full diagnostic panel including complete blood count, serum biochemical profile, and urinalysis should also be performed as early as possible to aid in identification of comorbid conditions and organ dysfunction(s), as well as to direct additional diagnostics. In addition, coagulation testing and a blood smear (or complete blood count) for platelet estimate are indicated before taking a patient to surgery.

Replacement fluid options for volume expansion include isotonic crystalloid solutions (0.9% saline; lactated Ringer's solution; Plasma‐Lyte A, Baxter Healthcare Ltd; Normosol‐R, Hospira, Inc.; hypertonic crystalloid solution; 7–7.5% saline; colloids e.g., hetastarch), blood and plasma products. The initial choice of fluid type depends largely on the cause of hypovolemia,

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