Complications
Reduced cardiac output commonly causes a decrease in renal perfusion leading to oliguria or anuria.[164]
Although AKI is relatively common, it is rarely associated with histological changes or with a need for long-term renal replacement therapy.
Reversal of oliguria can usually be achieved by the correction of volume depletion and hypotension.[164] A prospective cohort study indicated that high lactate, low diastolic blood pressure, high central venous pressure, and low systemic vascular resistance index on cardiac output monitoring at presentation to intensive care can predict the occurrence of AKI with 94% accuracy.[86]
Usually transient and not usually severe. It rarely results in death.[165] Circulating myocardial depressant factors are thought to be the cause.
After adequate fluid resuscitation, vasoactive-inotropic agents should be considered to maintain an adequate cardiac index, mean arterial pressure, mixed venous oxygen saturation, and urine output. Early use of vasoactive-inotropes in fluid refractory shock has been shown to improve outcomes.[95][134]
Clinicians should titrate treatment according to specific goals and desired endpoints. Endpoints should be refined at frequent intervals as the patient's clinical status changes.[165]
Patients with coagulopathy and DIC require maintenance of a normal platelet count and INR.
There have been no trials on transfusion of platelets and clotting components in children for DIC and coagulopathy in sepsis. It is prudent to treat symptomatically to avoid bleeding.
Platelets should be transfused to maintain the platelet count >50,000/microlitre to reduce the risk of spontaneous intracranial bleeding. Fresh frozen plasma should also be given to normalise the INR. Cryoprecipitate has a higher concentration of factor VIII and fibrinogen and can be used to treat hypofibrinogenaemia.
Glycogen stores can become depleted in sepsis; therefore, it is important to monitor for and treat hypoglycaemia with a continuous infusion of intravenous dextrose to provide age-appropriate glucose delivery (e.g., 2 mL/kg of 10% intravenous dextrose, followed by maintenance infusion at standard maintenance fluid requirement).[95]
Hyperglycaemia is common as part of the stress response to sepsis or as a side effect of corticosteroid treatment.
Although hyperglycaemia is known to be associated with adverse outcomes in multiple clinical settings (including paediatric intensive care), a firm recommendation for glycaemic control is yet to emerge from the scientific literature.[85] Current practice regarding management of hyperglycaemia in this setting varies among institutions, but tight control (i.e., treatment to target blood glucose of 4.0-7.0 mmol/L (72-126 mg/dL) did not improve major clinical outcomes while increasing the risk of hypoglycaemia.[85] Some experts introduce continuous insulin infusion if 2 consecutive blood glucose levels exceed 12 mmol/L (216 mg/dL) if the patient is in paediatric intensive care.
Sepsis, the systemic inflammatory response syndrome, and multi-organ failure are risk factors for acquired neuromuscular weakness.[167]
Neuromuscular weakness is related to the duration of immobilisation and is associated with the use of corticosteroids, sedation, and neuromuscular blockade.
Specialist investigations such as electrophysiological studies, imaging, and biopsies may be required to differentiate it from other causes of weakness or paralysis (such as compartment syndrome or cerebral infarct).
The pathophysiology of NEC is not fully understood. It appears to be a multifactorial and multisystem disease.[168] Risk factors include intestinal immaturity, inappropriate gut microbiota colonisation, hypoxia/ischaemia, feeding with artificial formula, and elective packed red cell transfusion. The mean prevalence among infants with a birth weight of 500 g to 1500 g is 7%, with an estimated mortality between 20% and 30%.[168]
The classical presentation of NEC would be a premature infant developing bilious gastric aspirate and emesis, abdominal distention, and blood in the stools following an increase in volume of enteral feeding.
Abdominal imaging may include pneumatosis intestinalis, gas in the hepatobiliary tree, and pneumoperitoneum.
Management of NEC involves conservative medical treatment with combination broad-spectrum intravenous antibiotics and bowel rest. Surgical intervention is required in patients with intestinal perforation and may involve laparotomy with resection of diseased or necrotic bowel, and enterostomy with creation of a stoma. Infants may develop small bowel obstruction secondary to bowel stricture during recovery.
Survivors of NEC are at substantially increased risk of long-term neurodevelopmental problems. Other long-term complications include requirement for long-term parenteral nutrition and short bowel syndrome.
Treatment of multi-organ failure in sepsis is primarily supportive. It includes effective antibiotic therapy, goal-directed therapy (to reverse hypotension, anaemia, coagulopathy, bleeding, and shock), and standard supportive intensive care unit care. This may include ventilatory support, sedation, and renal replacement therapy.
Acidaemia and hypoxia caused by sepsis can lead to pulmonary artery hypertension and persistence of the ductus arteriosus.
The increased right ventricular workload can lead to right ventricular failure with hepatic congestion and reduced cardiac output.
Mixing of de-oxygenated blood from the pulmonary artery with oxygenated blood in the aorta via the ductus arteriosus leads to differential oxygen saturations between the right arm and lower limbs.
Treatment includes inhaled nitric oxide and/or inotropic support.
Hypocalcaemia is common in children requiring intensive care unit admission for sepsis or septic shock.
Consensus guidelines for the treatment of septic shock in children include a recommendation for the correction of metabolic abnormalities, including hypocalcaemia. This recommendation is not based on specific evidence from randomised controlled trials; however, hypocalcaemia is recognised as a contributor to poor cardiac function.[169] Caution is advised when administering blood transfusions, as plasma calcium levels may be reduced by the citrate used for blood storage.
In terms of treatment, intravenous administration of calcium gluconate 10% is recommended.
Caused by raised intra-abdominal pressure (IAP) from factors such as bowel oedema and ascites. Abdominal organ perfusion becomes compromised if the mean arterial pressure cannot compensate for rising IAP.
Monitor with intra-bladder pressure through a Foley catheter. For IAP >12 mmHg, treat with diuretics, fluid removal with haemofiltration, or peritoneal drainage. In extreme circumstances (IAP >30 mmHg), surgical abdominal decompression may be required to restore abdominal organ perfusion.
When there is evidence of low cardiac output or cardiac index, thyroid function should be measured and thyroid replacement therapy initiated if there is evidence of thyroid insufficiency (i.e., elevated serum thyroid-stimulating hormone level or free serum T4 is low). Patients with sick euthyroid syndrome do not benefit from thyroid replacement therapy.
Focal neurological deficits and hearing loss are known complications of patients with bacterial meningitis but sepsis itself (of other origins) can also lead to permanent neurological impairment in very low birth weight infants.[166] The mortality and morbidity is higher for pneumococcal meningitis than for meningococcal meningitis.
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