Sepsis: A Clinical Guide

Written By Danial Mirza

Definition

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection (1). This modern definition, established by the Sepsis-3 consensus, shifts the focus from systemic inflammation to the presence of organ failure, highlighting the immediate severity and risk of mortality from the moment of diagnosis (1, 4).

Epidemiology

Sepsis is a major public health crisis, both in Malaysia and globally. It is consistently cited as the leading cause of admission to Intensive Care Units (ICUs) across Malaysia (20). Local data reveals a stark reality: the Malaysian Registry of Intensive Care (MRIC) reported an in-hospital mortality rate of 51.2% for sepsis in 2015, and other studies have found this figure to be in excess of 50% (20, 32). The elderly are particularly vulnerable, with one Malaysian study identifying a 30-day mortality rate of 50% in septic patients aged 65 and over, more than double that of younger patients (20).

Globally, the burden is immense. A 2020 study estimated 48.9 million cases and 11 million deaths from sepsis in 2017, accounting for approximately 20% of all global deaths for that year (22). The disproportionate impact on lower-middle-income countries underscores the global health inequity of this condition (22).

Pathophysiology

Sepsis is a syndrome of a runaway immune response. The process begins when immune cells recognize pathogen-associated molecular patterns (PAMPs), like endotoxin from Gram-negative bacteria, via receptors such as Toll-like receptors (TLRs) (5, 10). This triggers a cascade, activating transcription factors like NF-κB and unleashing a "cytokine storm" of pro-inflammatory mediators, including TNF-α, IL-1, and IL-6 (5, 10).

This overwhelming inflammation leads to widespread endothelial dysfunction. The endothelium produces excessive nitric oxide, causing systemic vasodilation and profound hypotension (10). Simultaneously, it becomes permeable, resulting in a massive "capillary leak" of fluid into the tissues, which causes edema and depletes intravascular volume (5, 13). Sepsis also induces a procoagulant state, leading to the formation of microthrombi throughout the microvasculature, a condition known as Sepsis-Induced Coagulopathy (SIC) or Disseminated Intravascular Coagulation (DIC) (5). This combination of distributive shock, microcirculatory failure, and cellular hypoxia forces a switch to anaerobic metabolism, producing lactic acid. The culmination of these insults is Multi-Organ Dysfunction Syndrome (MODS), the final common pathway to death (10, 19).

Clinical Presentation

Sepsis presents as a constellation of signs reflecting systemic inflammation and organ dysfunction. A high index of suspicion is crucial.

Diagnostic Clues

The quick SOFA (qSOFA) score is a rapid bedside tool to identify high-risk patients, using three criteria: altered mentation (GCS < 15), respiratory rate ≥ 22/min, and systolic blood pressure ≤ 100 mmHg. A score of ≥2 should trigger urgent further investigation (2).

Common Symptoms (>50%)

  • Altered Mental Status: Confusion, lethargy, or agitation is a key and often early sign, especially in the elderly (9).

  • Tachypnea (Respiratory Rate ≥ 22/min): A common compensatory response to metabolic acidosis (2).

  • Tachycardia (Heart Rate > 90/min): A classic sign of the stress response (15).

  • Fever (>38.3°C) or Hypothermia (<36°C): A core feature of the dysregulated inflammatory response. Hypothermia is an ominous sign (15).

  • Hypotension (SBP ≤ 100 mmHg): Indicates circulatory failure (2).

Less Common Symptoms (10-50%)

  • Chills and Rigors: Often indicates bacteremia (7).

  • Extreme Pain or Discomfort: A feeling of being "extremely ill" is common (13).

  • Clammy or Sweaty Skin: Can be warm and flushed initially ("warm shock") or cool and pale later (7).

⚠️ Red Flag Signs & Symptoms

  • Any acute change in mental status from baseline.

  • Hypotension unresponsive to initial fluid resuscitation.

  • Mottled skin, cyanosis, or prolonged capillary refill time, indicating poor tissue perfusion (10).

  • Acute oliguria (urine output <0.5 mL/kg/hr) or anuria, signaling acute kidney injury (13).

  • A non-blanching petechial or purpuric rash, which is a medical emergency suggestive of meningococcemia (74).

  • Pain out of proportion to visible skin changes, which may indicate necrotizing fasciitis (89).

Complications

Sepsis can lead to the failure of any organ system.

  • Respiratory: Acute Respiratory Distress Syndrome (ARDS)

  • Cardiovascular: Septic cardiomyopathy, refractory shock

  • Renal: Acute Kidney Injury (AKI) requiring dialysis

  • Neurological: Septic encephalopathy, coma

  • Hematological: Disseminated Intravascular Coagulation (DIC) with bleeding

  • Hepatic: Liver failure with jaundice

Prognosis

The prognosis for sepsis is grave, particularly once shock develops. In-hospital mortality in Malaysia exceeds 50% (20). For patients meeting the clinical criteria for septic shock (persistent hypotension requiring vasopressors and lactate >2 mmol/L), mortality rates can be over 40% (6). Key factors influencing prognosis include the patient's age, underlying comorbidities, the timeliness of antibiotic administration, and effective source control (20, 23).

Differential Diagnosis

[Severe Dengue]: This is a critical differential in Malaysia, as dengue shock can mimic septic shock. Shared features include fever, hypotension, and thrombocytopenia. However, dengue is suggested by the presence of severe retro-orbital pain, a characteristic "white islands in a sea of red" rash, and a positive tourniquet test. A markedly elevated hematocrit due to plasma leakage is a key laboratory finding in dengue, whereas hemodilution is more common in sepsis (54, 55).

[Melioidosis (Burkholderia pseudomallei)]: This should be considered in any septic patient in Malaysia, especially those with diabetes or from rural areas. It can present as pneumonia (often with upper lobe cavitation mimicking tuberculosis), multiple visceral abscesses, or fulminant septicemia. Standard empirical antibiotic regimens may not provide adequate coverage, making it a crucial differential to consider early (43, 48).

[Leptospirosis]: Consider this in patients with a history of exposure to floodwaters or contaminated water. The classic presentation includes high fever, severe myalgia (especially in the calves), and conjunctival suffusion (red eyes without discharge). Severe disease (Weil's disease) causes jaundice and renal failure, presenting as a sepsis syndrome (52).

Investigations

Investigations must be performed rapidly to confirm the diagnosis, identify the source, and guide therapy.

Immediate & Bedside Tests

  • Blood Gas Analysis (Arterial or Venous): This is an essential first test to measure lactate (a key marker of tissue hypoperfusion and a criterion for septic shock), pH, and bicarbonate to assess for metabolic acidosis (9).

  • Capillary Blood Glucose: An immediate fingerstick test is crucial as both hyperglycemia and hypoglycemia can occur and cause altered mental status (11).

  • Pulse Oximetry: This is a mandatory "fifth vital sign" to detect hypoxemia, which is a critical sign of respiratory dysfunction (6).

Diagnostic Workup

  • First-Line Investigations:

    • Blood Cultures: An urgent set of at least two pairs of blood cultures from separate venipuncture sites is essential to identify the causative organism (the rationale), which is the single most important step for guiding targeted antibiotic therapy and enabling de-escalation (the action) (10). These must be drawn before administering antibiotics, provided it does not cause significant delay (11).

    • Full Blood Count (FBC): This is required to identify thrombocytopenia (low platelets) (the rationale), which is a component of the SOFA score and a sign of sepsis-induced coagulopathy (the action) (11).

    • Renal and Liver Profiles: An urgent check of creatinine and bilirubin is mandatory to calculate the SOFA score (the rationale), which is necessary to formally diagnose sepsis and quantify the degree of organ dysfunction (the action) (2, 10).

  • Gold Standard: While there is no single gold standard test for the sepsis syndrome itself, positive cultures from a sterile site (e.g., blood or CSF) in a patient with clinical evidence of organ dysfunction is considered definitive proof of infection causing sepsis (the rationale), confirming the diagnosis and guiding specific treatment (the action).

  • Monitoring & Staging:

    • C-Reactive Protein (CRP) and Procalcitonin (PCT): Serial measurement of these inflammatory markers is performed to monitor the patient's response to treatment (the action), as a falling trend, particularly in PCT, provides objective evidence to support the safe discontinuation of antibiotics (the rationale) (28).

    • Chest X-Ray: A portable chest x-ray is a mandatory investigation for any septic patient with respiratory symptoms to identify a pulmonary source like pneumonia (the rationale), which is the most common cause of sepsis and requires specific management (the action) (10).

Management

Management Principles

The management of sepsis is a time-critical emergency focused on early recognition, rapid restoration of tissue perfusion, prompt antimicrobial administration, and definitive source control.

Acute Stabilisation (The First Hour)

The Surviving Sepsis Campaign "Hour-1 Bundle" provides a clear, actionable framework (95).

  • Circulation: Secure two large-bore IV cannulas and administer a stat fluid bolus of IV balanced crystalloids (e.g., Hartmann's solution) at 30mL/kg (the action) to rapidly correct hypotension and restore tissue perfusion, which is the primary goal of initial resuscitation (the rationale) (95).

  • Breathing/Airway: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 >94% (the action), which is crucial to prevent tissue hypoxia driven by the underlying pathology (the rationale) (6).

  • Disability: Continuously monitor neurological status (GCS) as septic encephalopathy is a sign of severe organ dysfunction (2).

Definitive Therapy

  • First-Line Treatment (Antimicrobials): The immediate administration of broad-spectrum intravenous antibiotics, ideally within one hour of recognition, is the single most important intervention to improve survival (95). The empirical choice must be guided by the suspected source, patient risk factors, and, crucially, the local hospital antibiogram and the Malaysian National Antimicrobial Guideline (NAG) (28). For community-acquired sepsis of unknown origin, a broad-spectrum agent like IV Piperacillin/Tazobactam is a common choice. For hospital-acquired sepsis, broader coverage with a carbapenem (e.g., IV Meropenem) plus Vancomycin is often necessary (28). Crucially, if melioidosis is suspected, the regimen must include IV Ceftazidime (43).

  • Second-Line/Escalation (Vasopressors): If hypotension persists despite the 30mL/kg fluid bolus (MAP < 65 mmHg), start an infusion of IV Norepinephrine (the action), as it is the first-line vasopressor to restore mean arterial pressure and ensure vital organ perfusion (the rationale) (97).

  • Source Control: This is a critical and concurrent priority. It involves the physical removal of the infection source, such as surgical drainage of an abscess or removal of an infected central line (the action), because medical therapy alone will fail if a nidus of infection remains (the rationale) (11).

Supportive & Symptomatic Care

  • Analgesia: Provide adequate pain relief.

  • Glycemic Control: Start an insulin infusion if blood glucose is persistently >10 mmol/L, targeting a range of 8-10 mmol/L (94).

  • Prophylaxis: Initiate VTE prophylaxis (e.g., subcutaneous heparin) and stress ulcer prophylaxis in eligible patients (97).

Key Nursing & Monitoring Instructions

  • Strict hourly input/output chart monitoring.

  • Hourly vital signs and neurological observations for the first 6 hours.

  • Inform medical staff immediately if systolic BP drops below 90 mmHg, urine output is <0.5mL/kg/hr, or there is any new deterioration in GCS.

  • Remeasure lactate within 2-4 hours to guide resuscitation.

Long-Term Plan & Patient Education

Discharge planning must address the high risk of Post-Sepsis Syndrome (PSS), a constellation of long-term physical, cognitive, and psychological impairments affecting up to 50% of survivors (7). Educate the patient and family about potential issues like chronic fatigue, "brain fog," anxiety, and PTSD. Provide referrals for physiotherapy, occupational therapy, and psychological support to facilitate a holistic recovery.

When to Escalate

Call Your Senior (MO/Specialist) if:

  • The patient meets the criteria for septic shock (requires vasopressors and has lactate >2 mmol/L).

  • The patient develops any new neurological signs or a drop in GCS.

  • Lactate fails to clear by at least 10-20% after 2 hours of resuscitation.

  • The source of sepsis is unclear or requires urgent specialist intervention (e.g., suspected necrotizing fasciitis).

  • There is any concern about the patient's trajectory or you feel out of your depth.

Referral Criteria:

  • Refer to the Intensive Care Unit (ICU) for any patient requiring vasopressors or invasive respiratory support.

  • Refer to the relevant Surgical team urgently for any source that requires procedural source control (e.g., abscess, bowel perforation, cholecystitis).

  • Refer to the Nephrology team if acute kidney injury does not resolve or requires renal replacement therapy.

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Danial Mirza
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