Shock - Septic: Nursing

Shock is a life-threatening condition that occurs when body organs don’t receive enough oxygen and nutrients for them to function properly. Shock can be grouped into four types based on the cause: hypovolemic, cardiogenic, obstructive, and distributive shock. And septic shock is a type of distributive shock that occurs secondary to sepsis, which is when the body mounts an excessive inflammatory response because of an infection.

Now, to understand distributive shock, let’s quickly review the physiology of blood vessels, which contain smooth muscle in their walls. When the smooth muscle relaxes, it increases the diameter of blood vessels, called vasodilation. On the other hand, when smooth muscle contracts, that decreases the diameter of blood vessels, called vasoconstriction.

The contraction and relaxation of smooth muscle is primarily controlled by the sympathetic nervous system, which normally maintains a partial constriction, generating enough force to keep blood moving through the circulatory system. The sympathetic system stimulation can increase or decrease to keep up with the body’s needs. Increased sympathetic stimulation of the blood vessels causes vasoconstriction, which leads to increased mean arterial pressure, or MAP for short. Vasoconstriction, when the total blood volume is constant, raises blood pressure and allows blood to flow faster through the blood vessels.

In contrast, vasodilation is typically caused by decreased sympathetic stimulation, in addition to inflammatory cytokines and histamine, which decrease mean arterial pressure. So, vasodilatation, when blood volume is constant, lowers the blood pressure and slows down the blood flow through the blood vessels.

Alright, now the main cause of septic shock is infections, particularly those caused by gram positive bacteria, like Staphylococcus aureus, Streptococcus pneumoniae or Enterococcus species, and gram-negative bacteria, like Escherichia coli. In addition to bacteria, infections caused by viruses, fungi, or parasites can also cause septic shock.

Typically, risk factors for developing septic shock include clients who are immunocompromised. This includes clients who are in the extremes of age, such as children and the elderly, as well as in clients with diabetes, chronic kidney or liver disease, as well as clients with an underlying HIV infection, those with chronic glucocorticoid treatment, and those with cancer who are being treated with chemotherapy. Other risk factors include prolonged hospitalization, indwelling catheters, as well as major surgery, and large open wounds.

Alright, now the pathological process of septic shock starts when a pathogen, say a gram-negative bacteria, enters the body and finds its way into the bloodstream. Embedded within the outer wall of this bacteria, there are types of lipopolysaccharides called endotoxins. These endotoxins are released when the Gram negative bacteria are destroyed by the immune system, which activates immune cells. In turn, immune cells release proinflammatory cytokines, like interleukins and tumor necrosis factor, or TNF for short.

These proinflammatory cytokines trigger excessive and widespread inflammation, called systemic inflammatory response syndrome, or SIRS. This response causes increased production and release of stress hormones, like catecholamines and glucocorticoids, as well as a response in the hypothalamus, blood vessel walls, as well as the capillary endothelial cells. Increased levels of stress hormones cause tachycardia and tachypnea, as well as increased production of white blood cells, or WBCs. On the other hand, some of these proinflammatory cytokines act as pyrogens. This means that they act on the hypothalamus to raise core body temperature above the normal set-point, which causes a fever.

Next, the vessel walls start producing nitric oxide, or NO for short, which is a vasodilator. Finally, the capillary endothelial cells refer to a decreased response to vasoconstricting stimulation, as well as a breakdown of the endothelial barrier, which increases permeability of blood vessels. This causes fluid to move from the vessels into the interstitial space, resulting in systemic hypotension. In addition, the endothelial cells attract more platelets, which stick into the endothelial cells, forming tiny clots called microvascular thrombi. All of these changes in SIRS decrease tissue perfusion, which causes tissue hypoxia.

Now, the next events in septic shock are grouped into four stages: initial, compensatory, progressive, and refractory stages. In the initial stage, systemic vasodilation causes less blood to return to the heart through the venous system; this, in turn, decreases cardiac output. As a consequence, body cells are not well-perfused, so they switch to anaerobic metabolism to produce energy, causing lactic acid to build up in the blood. When lactic acid builds up, that lowers blood pH, causing metabolic acidosis. This activates the compensatory stage.

During the compensatory stage, the sympathetic nervous system increases its activity to compensate for the decreased tissue perfusion in order to maintain homeostasis, and acid-base compensatory mechanisms activate to correct the acidosis. In the progressive stage, these compensatory mechanisms start failing , so the body’s metabolic needs can’t be met. This results in lactic acid buildup in the blood, more than in the initial stage, and gradually worsening metabolic acidosis. Finally, the refractory stage is when shock progresses to cellular death and multiple organ damage, which can be fatal.

Complications of septic shock include acute respiratory distress syndrome, or ARDS, disseminated intravascular coagulation, or DIC, in addition to multiple organ dysfunction syndrome, or MODS for short.

Signs and symptoms of septic shock can be grouped into early or late clinical manifestations. On a side note, early on, body temperature can be high but also low or normal. Early clinical manifestations can also include confusion or agitation, warm and flushed skin, respiratory crackles and tachypnea; in addition to a PaO2 below 60%; and tachycardia. There can also be signs of the initial infection, like a cough in case of pneumonia, or purulent discharge in a wound.

In contrast, late clinical manifestations include hypotension; delayed capillary refill; cool and mottled skin; gastrointestinal dysfunction, which can manifest as gastrointestinal bleeding or paralytic ileus and absent bowel sounds; in addition to oliguria. If the client develops ARDS, there can also be dyspnea and shortness of breath.

The diagnosis of septic shock starts with the client's history and physical assessment, followed by blood tests. These tests include CBC which can show leukocytosis and neutrophilia with a left shift, meaning more immature neutrophils in the blood; as well as thrombocytopenia. A comprehensive metabolic panel, or CMP for short, can show hyperglycemia, and high levels of creatinine, bilirubin and lactate. Coagulation studies and serum electrolyte levels can be abnormal, and other laboratory findings include increased inflammatory markers, like CRP and procalcitonin, and low levels of arterial oxygen.

Blood cultures, stool and urine cultures, cultures from indwelling catheters, as well as cultures from infected skin lesions can also be done, to pin down the causative organism and determine the most effective treatment option. Additionally, an electrocardiogram, as well as imaging studies like an X-ray or CT scan, can be done to determine the underlying cause of infection.