Septic shock

Sepsis/septic shock is a serious type of distributive shock caused by a dysregulated and overwhelming host response to infection (Singer et al., 2016). In this type of shock, pathogens such as gram negative bacteria and their microbial products, for example lipopolysaccharides (LPS), cause a highly immunogenic and toxic molecule to activate the inflammatory system – the body’s natural response to injury (in this case injury to the endothelial system). However, microbial toxins and activated inflammatory cytokines from the inflammatory pathway cause vasodilatation and low systematic vascular resistance (SVR), i.e., poor vessel tone, which increases vessel permeability, causing fluid to leak out of the circulatory system. SVR refers to the resistance offered by all blood vessels to the aortic valve when it opens to eject blood. Low SVR can be caused by the host (child’s) own response to inflammation – the systemic inflammatory response syndrome (SIRS). Inflammatory mediators (e.g., cytokines, interleukins) and bacterial toxins (e.g., LPS) cause dilatation of blood vessels and lead to low SVR, also known as warm shock.

In septic shock, 20% of patients will present with this type of warm shock. Other features of warm shock are tachycardia, bounding peripheral pulses, and a warm skin. Warm shock results in high cardiac output and low SVR. These children require proper management as they may decompensate into shock with hypotension secondary to low SVR. Alternatively, they may quickly decompensate into cold shock, which is more difficult to treat. Eighty percent of children in septic shock present with features of cold (or late) shock. In cold shock, the child becomes excessively vasoconstricted, skin is pale, cool or cold to touch with mottling as blood is shunted away and capillary refill time is prolonged. This sympathetically mediated response maintains the child’s blood pressure for a while until there is decompensation and the child collapses. By this stage, capillary blood flow becomes sluggish, capillaries become leaky and permeable, there is third‐spacing of fluid further exacerbating the hypovolaemic state, and metabolic acidosis. Cold shock is associated with low cardiac output, high SVR and poor outcome. Refractory shock is defined by irreversible shock, multi‐organ failure and death.

Initially, as a compensatory mechanism, blood vessels try to maintain tone, which is one of the major differences between adults and children as children will maintain their SVR and blood pressure until the pre‐terminal stage. During the compensatory stage, however, you may observe a subtle increase in diastolic blood pressure and a subtle decrease in pulse pressure (difference between systolic and diastolic blood pressure), which results in a normal systolic blood pressure. Monitoring the trends in blood pressure is therefore an important nursing skill and a vital part of nursing practice, and such observations are key to identifying shock at an early stage. This is usually coupled with an early rise in heart rate (tachycardia) to maintain the circulating volume. In almost all types of shock, the body attempts to improve its cardiac output and circulating volume by activating the sympathetic nervous system and it releases endogenous catecholamines, such as adrenaline and noradrenaline, which increase cardiac contractility and heart rate. This is the reason for an early rise in heart rate. Thus a very obvious early sign of any type of shock is tachycardia. Other signs of early shock are warm skin tone, flushed appearance (usually also fever), flash capillary refill time, and bounding pulses. These are signs of a hyperdynamic circulation and fluid resuscitation during this stage may reverse these early symptoms.

Here, the inflammatory response can become so extreme and the vessel tone so excessively dilated that it is not uncommon to volume resuscitate a child to over 100 ml/kg of fluid. This is severe distributive shock caused by sepsis and inflammation, and by this stage the child will have been referred to or transferred to the ICU for intensive care management. This life‐threatening emergency presents with features of cold shock: cool or cold peripheries, cyanosed or mottled skin, prolonged capillary refill, oligo‐anuria, metabolic acidosis, tachycardia and hypotension. These children are extremely ill and can develop a serious condition known as disseminated intravascular coagulopathy (DIC).

DIC is an over‐activation of the inflammatory and clotting system. Any type of injury, including injury to the endothelial system as in shock, will activate both these systems. The inflammatory system aims to protect the organism while the clotting cascade aims to heal and seal the vessel or injured area. However, in DIC the clotting system also becomes deranged because sepsis is a condition of extensive and ongoing microvascular injury and clotting products become so quickly consumed that it becomes difficult to replace them.

Another complication of DIC is not only the resulting coagulopathy but also the microvascular clotting and fibrin deposits that occur in the small blood vessels, which then occlude tissues from extracting oxygen. As aerobic metabolism requires oxygen, tissue dysoxia initially leads to anaerobic metabolism, metabolic acidosis and a rise in lactate – the by‐product of anaerobic metabolism – all of which will eventually lead to cell death. That is why DIC is a marker of poor prognosis and is associated with the mnemonic Death Is Coming (Moore, Knight & Blann, 2016). Thus DIC is both a clotting and bleeding disorder that is difficult to treat. The underlying condition, i.e., the stimulus for DIC, in this case sepsis, must instead be treated and controlled. Treatment of DIC is therefore only symptomatic and patients will require many blood and blood product transfusions. These patients are usually cared for in the paediatric intensive care unit (PICU). Fortunately, the majority of children with sepsis and septic shock do recover to lead normal lives. International efforts such as the Surviving Sepsis Campaign and Sepsis 6 (NICE, 2016) aim to improve diagnosis and survival rates of children with sepsis through early recognition and timely treatment. Thus, nurses and other healthcare professionals play a vital role in recognising and reporting the signs and symptoms of sepsis early so that children are given the best chance of survival.

See Table 6.2 for an overview of SIRS to septic shock.

Although the early signs of compensated shock may be short‐lived, the clinical features of decompensated shock are very obvious. This is due to the vasoconstriction that comes from decompensated shock. Blood vessels will constrict so that the circulating volume is maintained and to shunt blood to vital organs. Such vasoconstriction will manifest as cold, clammy skin, mottling, there may be floppiness and poor muscle tone in infants and young children, and persisting tachycardia.

Tachycardia will decompensate further into bradycardia, a pre‐terminal sign, if this stage is not adequately or promptly managed. In decompensated shock, capillary refill time is prolonged and there may be low rather than high core temperature. Unlike adults who become hypotensive at an early stage, children will remain normotensive but significantly tachycardic until they become pre‐terminal. As blood flow is diverted from the kidneys to more vital organs, there may be oliguria or anuria and poor perfusion to other non‐vital organs, for example, gut. Urine output less than 1 ml/kg/h in young children and less than 0.5 ml/kg in older adolescents must be reported in a timely manner as this is a very serious but early feature of poor kidney blood flow and perfusion. Monitoring urine output and maintaining an accurate fluid balance chart is therefore a vital part of the nurse’s role.

Cold shock from any cause is a more severe type of shock and is more difficult to treat. It is a life‐threatening condition, requires invasive monitoring and intensive care drugs only possible in PICU. Regardless of the type of shock, however, all patients suspected of being septic must have appropriate antibiotics administered without delay as this can be life‐saving (Dellinger et al., 2013).

The clinical features of warm and cold shock are highlighted in Fig. 6.1.

Life‐threatening complications related to septic shock are outlined in Fig. 6.2.

Neurogenic shock

Another type of distributive shock is neurogenic shock. Neurogenic shock is caused by the sudden loss of autonomic control and impairment of autoregulation resulting from spinal cord injury (SCI) – especially above T6. Here, disruption to the descending pathways of the sympathetic nervous system results in unopposed vagal (parasympathetic) tone. Loss of tone and dilatation of vascular smooth muscles and an increased venous capacitance results in a decreased SVR. There will be a relative hypovolaemia, meaning that the circulating volume in itself is unchanged but as the blood vessel capacity enlarges, the existing circulating volume becomes inadequate to fill it. The relative hypovolaemia and the disruption to vessel autoregulation result in hypotension.

Neurogenic shock is managed with fluids and drugs that aim to increase the tone of blood vessels. The treatment should support blood pressure until the patient overcomes and the body has time to adapt to the changed system due to the SCI. Bradycardia, another consequence of neurochemical derangement and autonomic dysregulation in SCI, should also be managed with drugs such as atropine or glycopyrrolate. These drugs can be given prophylactically prior to suctioning or turning the patient if they are particularly sensitive to these interventions, which may cause a vagal response. Other dysrhythmias are also possible in severe conditions and should be controlled for as cardiac dysrhythmias can cause poor ejection of blood out of the heart. Bowel and bladder care is important so that constipation or urinary retention, a distended abdomen and pain do not trigger an episode of neurogenic shock in these patients.

Neurogenic shock can occur anytime following injury up to 6 weeks post‐injury (Mack, 2013). There is no diagnostic test for this condition so history, the nature of spinal cord injury, and exclusion of other causes for hypotension and bradycardia contribute to the diagnosis of neurogenic shock. Bradycardia in these patients is exacerbated by any condition that increases intra‐cranial pressure, such as suctioning, defaecation, coughing, turning the patient, and hypoxia. Initially, the skin can be warm and flushed in this condition but heat loss from profound vasodilatation can cause hypothermia.