"When in continued fever, the external surface of the body is cold and internally great heat is felt; with thirst; the affection is mortal" (Hippocrates, 460–370 BC).

There are multiple detailed definitions of shock. Many years ago it was a purely clinical description based on tachycardia, pale mucous membranes, prolonged CRT, low blood pressure, and sometimes consciousness impairment.

With the advancement of molecular biology, a more modern definition would be a sudden failure in the peripheral circulation that may be caused due to insufficient vascular volume, loss of circulatory control, or lack of an adequate cardiac function.

Another definition has been "a critical imbalance between the delivery of oxygen and nutrients to the cell and utilization of oxygen and nutrients by the cell. Shock may be any syndrome, disease state, or injury that results in a critical decrease in effective blood flow that leads to derangement in cellular metabolism and ultimately cell death. Shock leads to multiple organ dysfunction and failure, and may culminate with death."

While many definitions were about the hemodynamic condition of the patient such as capillary refill time (CRT), mucous membranes (MM), arterial blood pressure (BP), central venous pressure (CVP), cardiac output (CO), a current tendency has put more emphasis on the microcirculation. Some research has found that there is a direct correlation between clinical parameters such as BP and the level of perfusion at the cellular level.

Thus, the final effects of shock may occur at a microcirculatory level leading to lack of oxygen and substrate delivery to the cells. Shortly after without oxygen, cells will no longer be able to produce ATP, losing the capability of maintaining normal homeostasis.

It has been estimated that the cell expends approximately 93% of the total ATP production on keeping up a "survival" level of homeostasis, so critical reductions in ATP's production may lead to necrosis or apoptosis. Also during this process, the cells are pushed to work under anaerobic glycolysis, resulting in the production of lactic acid and leading to elevated lactate levels and academia. The level of lactate can be used for diagnostic or prognosis purposes.

Functional classifications and examples of shock

Silverstein, LAVECCS, 2012

Another classical approach to describing shock in a more clinical mode has been using stages depending on presentation: compensatory (early), early decompensatory (middle), and late decompensatory. However, while this describes fairly appropriately what happens in dogs, cats seem to have a different process, and often you cannot recognize these stages in critical cats.

Septic shock is defined currently as a circulatory shock that is caused by the systemic body response to an underlying infectious agent. The presence of bacteria (infection) and the correspondent inflammatory response to that insult (sepsis) includes a very complex interaction between cells and molecules that includes inflammatory cell activation and mobilization, the release and activation of cytokines and enzymes (proteases, catalases), the activation of the complement system, the activation of the coagulation cascade, the active participation of many cellular populations as the endothelium, lymphocytes, macrophages, etc.

This complex and interconnected process leads to a large amount of biological responses and clinical consequences: impairment of the intracellular metabolism, decrease in myocardial contractibility, decrease in the cardiac output, and decreasing/increasing of vasomotor that leads to hypotension and/or impaired tissue perfusion. The GI tract may develop ulceration or hemorrhage due to the lack of proper perfusion for the formation of mucus, the kidneys may develop renal failure, the leak of albumin due to enlarged pore size in the endothelium increasing the permeability and may lead to reduced oncotic pressure, hypoproteinemia and hypovolemia.

The treatment of these patients is complex, requires a well-trained staff and monitoring capabilities, and results are often frustrating.

IV fluids through a large-bore, peripheral catheter should be installed. The usage of a central line (jugular catheter) is controversial due to possible thromboembolism. Multiple recommendations have been made for the "right" choice for fluid therapy. The classic approach with a "shock" dose of sodium-containing crystalloids at 80–90 ml/kg in dogs and 45–60 ml/kg in cats seems to produce higher mortalities. Colloids (plasma, hetastarch or dextrans) may be considered if the total protein is ≤ 3.5 g/dL or the albumin is < 2 g/dL. However, new information seems to relate the usage of colloid with higher mortalities due to kidney disease or coagulation issues.

We recommend thoracic radiographs and abdominal ultrasound if the source of the infection is not clear. If fluid collections are found, sampling and culture and sensitivity are indicated. In the meantime, antibiotic therapy should be instituted pending the results. See Table 1.

Other aspects of the therapy are:

 Use of antiulcer drugs such as famotidine, ranitidine or cimetidine trying to reduce the risk of ulceration.

 Providing nutritional support is critical in septic patients. Enteral nutrition is the ideal method.

 Control vomiting using maropitant or ondansetron (metoclopramide can be used, but there is certain controversy about it).

 Nursing care is essential for these patients: Recumbent patients should be turned every 4 hours for prevention of decubital ulcers, performing catheter maintenance, usage of towels or blankets, allowing resting time, minimizing the number of interventions, etc.

Table 1. Antibiotic dosages, route, and frequency used on septic patients

References

References are available upon request.