What Is Septic Shock?
Septic shock is a potentially fatal illness that develops after infection when the blood pressure drops to a life-threatening low level.
What Are the Symptoms of Septic Shock?
Sepsis is a medical emergency; however, its early symptoms frequently resemble those of other conditions, such as a cold or fever. The most commons symptoms of sepsis are:
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High fever.
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Bodyache.
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Increased heart rate.
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Increased breathing.
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Alteration in the mental status.
Sepsis turns into septic shock if medical intervention is not timely and appropriate. The additional symptoms seen during septic shock are:
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Low blood pressure.
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No or very low urine output.
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Limbs become cold and pale.
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Rashes appear.
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Palpitation of the heart.
What Is the Pathophysiology of Septic Shock?
Sepsis is a clinical condition that occurs along a continuum of pathophysiologic states. It begins with the systemic inflammatory response (SIRS) syndrome and concludes with the multiorgan dysfunction syndrome (MODS) just before death. The following indicate inflammation at its earliest stages:
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Fever (increase in body temperature).
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Tachycardia (increase in heart rate).
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Tachypnea (increase in respiratory rate).
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Leukocytosis (increase in white blood cell count).
For the diagnosis of systemic inflammatory response syndrome, two of these signs should be present simultaneously at the same time. If two of these signs are present along with an infectious source, the condition can be recognized as sepsis. Due to the development of hypotension, the tissue demand for oxygen increases and hence is not met by the body's oxygenation process. Cellular and metabolic abnormalities result from decreased peripheral vascular perfusion and oxygenation. The respiration process switches from aerobic to anaerobic resulting in lactic acidosis. Pre-renal azotemia and transaminitis are two examples of end-organ damage symptoms that can indicate tissue hypoperfusion.
Septic shock results when sepsis-induced hypotension is persistently resistant to initial therapy with fluid resuscitation. Histamine, serotonin, super-radicals, and lysosomal enzymes are some of the inflammatory mediators produced in response to bacterial endotoxins and cause a significant increase in capillary permeability and a corresponding decrease in peripheral vascular resistance. It causes a reduction in stroke volume, which is accommodated initially by elevation in the heart rate (compensated septic shock). As a result, the patient is in a hyperdynamic state (cardiac output increases above the normal level), characteristic of septic shock.
Clinically, patients exhibit a dynamic precordium (chest wall region) with bounding peripheral pulses and kidneys. The capillary refill reduces, and patients are warm to the touch. It is referred to as a warm shock. As shock advances, the body tries to divert blood from non-essential tissues. Higher catecholamine synthesis causes peripheral vascular resistance. This is referred to as cold shock.
Functionally, septic shock is characterized by prolonged hypotension despite the adequate fluid replacement of 60 to 80 mL/kg. Vasoactive medications like beta-adrenergic and alpha-adrenergic drugs are administered. The progression of organ malfunction characterizes multi-organ dysfunction syndrome despite administering high doses of vasoactive substances (MODS).
What Are the Changes Seen During Sepsis at Cellular Level?
Changes and abnormalities influence the sepsis pathophysiology in immune function, the endothelium, the intestinal epithelium and microbiota, and the coagulation cascade on a cellular and subcellular level.
Immune Dysfunction:
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Changes Seen in Innate Immunity - When a pathogen invades, the innate immune system is the first to recognize and respond to the early signals of infection. The infection is controlled by neutrophils, macrophages, natural killer cells, and complement proteins. Cytokines and chemokines are released, and the levels increase further in the presence of sepsis. Moreover, neutrophils emit reactive oxygen species and neutrophil extracellular traps, which play a part in the failure of many organs.
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Changes Seen in Adaptive Immunity - Sepsis causes a significant decrease in the lymphocyte population, with CD4+ T cells and B cells showing the greatest decrease in septic patients. The decreased cell count makes the patient more prone to nosocomial infections in sepsis. T-cell exhaustion markers, along with increased helper T-cells and regulatory T-cells, are seen. In addition, CD8 T-cells (cytotoxic T-cells) are reduced in number.
Inflammatory Reflex:
The vagal nerve fibers that control the immune response are called neuro-immune regulation. They are also known as inflammatory reflexes. The chemical mediators of inflammation and injury cause the triggering of afferent nerve fibers (the sensory nerve that carries sensory data to the brain). The vagus nerve then receives a signal from efferent fibers (carries information from the brain to organs), which causes the release of acetylcholine from the spleen. In addition, the cholinergic receptors present on the macrophages are activated, causing suppression in the release of cytokines (an inflammatory mediator).
Endothelium Changes:
The endothelium acts as a selective barrier to control water, solutes, and blood cell components transport to the tissues. The endothelium surface influences both vascular tone or permeability and immune response modulation by expressing immune receptors like TLRs (toll-like receptors that are expressed mainly on macrophages and dendritic cells). TLR signaling affects the expression of the coagulation pathway signaling and the permeability of endothelial cells resulting in coagulopathy, increased vascular permeability, and organ dysfunction in septic patients.
What Is the Management of Shock?
Controlling the Source of Infection:
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If the source of septic shock is any infected or necrotic tissue, it must be immediately removed. For example, patients with cellulitis, pus, abscess, and infected devices.
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Broad-spectrum antibiotics should be provided to the patients.
Management of Shock:
The symptoms of shock are managed by compensating for oxygen and putting the patients on ventilation. The central venous line has to be restored. Adrenergic drugs are given to the patient.
Host Response Enhancement:
Corticosteroids are provided to the patient to boost their immunity.
Conclusion:
Immunologic dissonance (exaggerated pro-inflammatory response) versus immunologic paralysis (exaggerated anti-inflammatory response) have been suggested to play a role in the poor prognosis and death, while the specific causes remain unclear. Despite all of the medical advancements, septic shock still has a high death rate that can surpass 40 percent. The type of organism, antibiotic sensitivity, number of damaged organs, and patient age are only a few of the many variables that determine mortality. The mortality increases with the number of factors that match SIRS. According to the data, tachypnea and changed mental status are strong indicators of unfavorable outcomes. People who survive have serious cognitive and functional disabilities.
