This chapter presents a case of an 89-year-old female with fever and altered mental status. The patient presents with systemic inflammatory response syndrome (SIRS) due to pneumonia. The case presents the medical interventions to mitigate progression to multiorgan dysfunction or septic shock.

This chapter describes a case of a 2-month-old male preterm infant who presented with emesis and blood in the diaper. The patient has a weak cry, labored breathing, and periodic apnea. The physical exam reveals abdominal distension, tenderness, and bloody stools, which are concerning for sepsis. The patient is diagnosed with necrotizing enterocolitis, a serious condition characterized by intestinal inflammation that may lead to intestinal perforation, bowel necrosis, and/or death. The initial work-up includes sepsis evaluation, blood, urine, CSF cultures, CBC, electrolytes, and blood gas. X-ray findings include diffuse pneumatosis intestinalis, and portal venous air, which are pathognomonic for necrotizing enterocolitis. The mainstays of therapy include bowel rest, bowel decompression, and broad-spectrum antibiotics. Pediatric surgery is consulted, and the patient admitted for IV antibiotics and possible exploratory laparotomy.

1. Initial assessment and stabilization of airway patency, breathing, and circulation should be performed.

2. It is important to have a high index of suspicion for adrenal insufficiency (AI) in cancer patients with refractory hypotension. AI can occur as a result of adrenal suppression from chronic glucocorticoid treatment, or less commonly, from metastatic disease to both adrenal glands.

3. Consider obtaining other laboratory work to evaluate for concomitant electrolyte abnormalities.

4. Review patient’s medication lists whenever accessible to evaluate for chronic steroid use.

5. Treatment involves resuscitation of blood pressure acutely with IV hydrocortisone and intravenous fluids followed by admission to the hospital.

A primary brain injury occurs at the time of initial mechanical trauma. An additional secondary brain injury begins immediately after impact. Inflammatory and neurotoxic processes result in raised intracranial pressure, decreased cerebral perfusion and ischaemia. This secondary injury is worsened by further physiological insults such as hypotension and hypoxia.

Assessment of the patient begins with an ABCD approach and should take place alongside resuscitation. Airway management is the priority, and this must be safely secured when indicated. Cervical spine injury is often associated with a head injury. The neck should be immobilised. Hypoventilation causes hypoxia and hypercapnia. Controlled ventilation to achieve a PaCO2 of 4.5 - 5 kPa and a PaO2 of > 13 kPa is recommended to control intracranial pressure. Hypotension reduces cerebral perfusion; a mean arterial pressure of > 90 mmHg should be targeted. Neurological assessment is undertaken using the Glasgow Coma Scale (GCS). A GCS less than 8 is considered a serious head injury and is often an indication for tracheal intubation. Other indications are described. Transfer to a neurosurgical unit is often required. Safe transfer guidelines must be followed.

Allergic reactions can occur with both anaesthetic drugs as well as other agents administered by the anaesthetist or surgeon. Common causes are antibiotics, neuromuscular blocking drugs, chlorhexidine and patent blue dye. Less common triggers include propofol, opioids and local anaesthetics.

Signs of a severe reaction include hypotension, bronchospasm, oedema (including laryngeal oedema) and cutaneous manifestations such erythema, and cardiac arrest. Not all signs are present. Management includes stopping the suspected agent followed by the ABC of resuscitation (100% oxygen), adrenaline (epinephrine) and 10-20 mls/kg of intravenous crystalloid. CPR may be required. Secondary management includes the use of steroids, bronchodilators and antihistamines.

Patients should have serial blood samples for serum tryptase and referred for investigation. Successful identification of the agent needs to be communicated to the patient (who needs to have written record or wear a Medic Alert bracelet) and clinical staff in primary and secondary care.

In perioperative medicine, optimal fluid management during and after the surgery is often debated. However, it is clear that poor fluid management and periods of hypotension are closely linked to worse outcomes. Both excessively liberal and restrictive fluid regimens lead to harm. Goal-directed pathways, where fluid or vasopressor administration targets a predefined hemodynamic parameter, are occasionally used. However, these require advanced hemodynamic monitoring, have limited evidence to support them and are often too complex, resulting in unsuccessful implementation.

Artificial intelligence (AI) focuses on machines capable of replicating human decision making. Within AI, predictive analytics use existing data to predict future events. These predictions can be integrated into open- or closed-loop systems, guiding fluid or vasopressor administration and reducing the clinician’s cognitive burden. This chapter provides an introduction to predictive analytics in perioperative fluid management, an overview of published literature, andsuggestions as to how the technology might develop in the future.

• Sepsis is currently defined as life-threatening organ dysfunction caused by dysregulated host response to infection. Septic shock is sepsis with persistent hypotension requiring vasopressor to maintain mean arterial pressure (MAP) ≥ 65 mmHg and having a serum lactate > 2 mmol/dL despite adequate fluid resuscitation.

There is wide variation in test characteristics for screening scores such as systemic inflammatory response syndrome (SIRS), quick Sequential Organ Failure Assessment (qSOFA), National Early Warning Score (NEWS) and Modified Early Warning Score (MEWS). A qSOFA score of ≥ 2 or a change in SOFA score of ≥ 2 can promptly identify these patients; however, qSOFA is not recommended as a single screening tool over comparable scores such as SIRS, NEWS, or MEWS.

Shock is a pathological state resulting from inadequate delivery, increased demand or poor utilization of metabolic substrates (i.e., oxygen and glucose), which leads to cellular dysfunction and cell death. This then leads to progressive acidosis, endothelial dysfunction and inflammatory cascade that results in end-organ injury. Early in the course of shock, compensatory mechanisms may attempt to augment cardiac output (CO) and/or systemic vascular resistance (SVR) in an effort to improve tissue perfusion. Without treatment, those compensatory mechanisms are overwhelmed, leading to decompensated shock, multiorgan failure (MOF) and death.

• Adrenal insufficiency can be either primary, resulting from destruction of the adrenal gland, or secondary, resulting from a deficiency of ACTH (adrenocorticotropic hormone, corticotropin).

• Adrenal crisis is either the acute development of severe adrenal insufficiency or a rapid deterioration from baseline chronic adrenal insufficiency (which is often insidious) brought on by a stressor.

• The adrenal gland (made up of cortex and medulla) produces three categories of steroids: glucocorticoids (cortisol), mineralocorticoids (aldosterone) and gonadocorticoids (sex hormones). Aldosterone levels change in response to volume status and sodium intake. Aldosterone maintains sodium and potassium concentration and regulates water balance.

In acute ischaemic stroke, cerebral blood flow autoregulatory mechanisms may be disrupted so that cerebral perfusion becomes reliant on systemic blood pressure. Too low blood pressure may lead to progression of the infarction and too high blood pressure may cause cerebral oedema or haemorrhagic transformation of the infarct. In patients with BP = 220/120 mm Hg who do not receive intravenous thrombolysis, it is reasonable to lower BP by 15% during the first 24 hours after stroke onset. Patients who have elevated blood pressure and are otherwise eligible for treatment with intravenous rt-PA should have their blood pressure lowered so that systolic blood pressure is < 185 mm Hg and their diastolic blood pressure is < 110 mm Hg before thrombolytic treatment is administered. Acute stroke patients should be assessed for dehydration and a fluid balance chart should be kept. Underlying causes of hypotension should be treated rapidly. There is no beneficial effect of hemodilution treatment for acute ischaemic stroke. Fibrinogen-depleting agents that reduce viscosity may marginally reduce risk of recurrent ischaemic stroke, but more greatly increases symptomatic intracranial haemorrhage. Methylxanthine derivatives such as pentoxyphylline and propenofylline that reduce viscosity and produce vasodilation have insufficient evidence to support their use.

Missatributing symptoms to already established conditions often represents a missed opportunity to improve management. These cases provide some examples.

Epidural analgesia is a safe and effective method of providing pain relief before, during and after a surgical procedure, or for patients with chronic pain, using a combination of local anaesthetic and opioids. The choice of agent, contraindications and complications of epidural analgesia are discussed, and the reader is also provided with top tips for prescribing epidurals.

Point-of-care transthoracic echocardiography (TTE) is integral to the practice of acute care medicine to help assess patients quickly, accurately, and non-invasively. This review discusses how point-of-care TTE works in terms of logistics and diagnostic capabilities, specifying the information available from each point-of-care TTE view. The TTE findings of potentially reversible causes of shock are also described to help distinguish different causes of shock and to guide management and therapeutic interventions. While data have not shown that point-of-care TTE improves patient outcomes or mortality, it can certainly narrow the differential diagnosis for the cause of shock, potentially allowing earlier, more appropriate treatment.