ICU care & monitoring + Sepsis + Shock + antibiotic + Burn + DKA 🔥🚨 Flashcards

(35 cards)

1
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Level of ICU care

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2
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Sepsis definition, SoFA & surviving sepsis campaigne

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3
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Overview of Sepsis

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4
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Management of Severe Sepsis ( Outline)

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approach using CCrISP protocol:
- ABCDE
- regarding resuscitation:
- Start with a rapid fluid challenge of 10 ml/kg warmed crystalloid in the normotensive
patient or 20 ml/kg if the patient is hypotensive. You should be more tentative in
patients with known cardiac dysfunction, starting with an initial bolus of 5 ml/kg.
Closer monitoring may be needed in these patients.

Initial resuscitation
* Early goal-directed therapy
* During first 6 hours
* Goals
1) CVP 8 – 12 cmH20
2) MAP ≥ 65 mmHg
3) U/O ≥ 0.5ml/kg/hr
4) Lactate normalised
5) SVC oxygenation 70%
* Although controversial, CVP is still used as there are not many objective, obtainable, reliable substitutes & a low CVP is indicative of hypovolaemia
* Ventilated or IAH patients, allow CVP 12 – 15cmH20 to account for filling impediment
* Widened pulse pressure is a good marker for hypovolaemia

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5
Q

Critical care

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  • Branch of medicine concern with life threatening condition requiring organ support and invasive monitoring.

This include:
* Monitoring
* Ventilation & oxygen therapy
* Specific organ support

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6
Q

Types of Monintoring in Critical care

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  • Divided into invasive and non invasive monitoring

- CNS
* Non invasive : GCS, pupil
* Invasive : ICP monitor, EVD

- CVS
* Non invasive : HR, NIBP, Cardiac monitor
* Invasive : CVP, IBP, Swanz catheter, Cardiac monitor via artline or CVL

- RESP
* Non invasive : SpO2, RR
* Invasive : ABG

- Renal
* Non invasive : -
* Invasive : Urine output, VBG, RP

- GIT
* Non invasive : BO, BMI, ABID
* Invasive : NG tube monitoring, IAP monitoring

-Endocrine : RBS, electrolyte
-Musculoskeletal : Observe for bedsore, contracture
-Hematology :Observe for DVT
-Microbiology : Daily review for antibiotic use

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7
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Respiratory support in Critical care

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  • Oxygen therapy is defined as administration of oxygen as medication
  • Divided into non invasive and invasive therapy

- Non invasive:
* Nasal Prong
* Face mask
* Venturi Mask
* Non rebreathable mask
* Head box
* NIPPV : CPAP (Continuous positive airway pressure) & BIPAP (Bilevel Positive Airway Pressure)

- Invasive
* Mechanical ventilation
* Iron Lung
* HFOV

- Surgical Procedure
* Tracheostomy

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8
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Cardiac support in critical care

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9
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Renal support in Critical care

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  • Indication for renal support
  • Persistent metabolic acidosis
  • Persistent hyperkalaemia
  • Oliguria or anuria

- Renal replacement therapy
HD : Continous venovenous hemodialysis
* Need dialysate for counter current. Not for unstable patient. 4 hour.

CVVH : Continous venovenous hemofiltration
* Convection of molecule through a permeable membrane. Waste filtered. For low bp, unstable bp. 24 hours

SLED
* Sustained low efficiency dialysis. Sslow dialysis 8 - 24 hd

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10
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Other systems monitoring in critical care

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GIT
- Nutritional support
- PPI & motility agents
- Probiotics and immunonutrition

HEMATO
- Anticoagulant
- Blood product

MUSCULOSKELETAL
- Bedsore prevention
- Early ambulation

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11
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Types of Shock

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12
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Prophylactic Antibiotic

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Duration of Prophylaxis
Limiting the duration of antibiotic prophylaxis reduces the risk of resistance and other complications:
• Single Dose: Often sufficient for most procedures.
• Extended Prophylaxis: In specific cases, such as cardiac or orthopedic surgeries involving implants, prophylaxis may continue for up to 24 hours postoperatively.
• Avoid Prolonged Use: Extending prophylaxis beyond 24 hours has not shown additional benefits and may increase risks.

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13
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What is Antibiogram

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ANTIBIOGRAM
- The result of a laboratory testing for the sensitivity of an isolated bacterial strain to different antibiotics. It is an in vitro sensitivity

GENERAL CONCEPT
- Microbiology sample are examine under microscope and bacteria is cultured.
- The aim is to obtain minimum inhibitory concentration(MIC) on antibiogram which is defined as lowest concentration of antimicrobial that will inhibit visible groth of microorganism after overnight incubation.
- MIC is used to determind amount of antibiotic needed and prevent resistance.

2 method of obtaining antibiogram:
Diffusion method (Kirby Bauer method)
* Disc with different abx are dropped on different area of agar plate. A disc of bacterial lysis will be visible based on sensitivity
* Diameter of disc is suggestive of MIC (minimal inhibitory concentration) → convert diameter in mm into MIC (µg/ml)

Dilution Method
* Series of antibiotic vial with progressive lower concentration of antibiotic are used.
* Test till the last vial on which no bacteria growth is the MIC

USE
- Assess the susceptibility rate
- Aid in selection of empirical antibiotic
- To monitor resistance trend over time
- To compare susceptibility and resistance between center.

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14
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Overview on staining

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15
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types of burn

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16
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Primary survey for burn

17
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resuscitation for burn

18
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thickness for burn

19
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Dressing for Burn patient prior to transfer

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mechanism of burn

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Burn Management (1)

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Burn Management (2)

23
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🔥 Acute Burn Management – Detailed Notes (MOH Malaysia 2024)

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📌 1. First Aid at the Scene

Goals: Stop burning, prevent progression, reduce complications

Key Steps:

  • ⚡ Ensure safety before helping (turn off power source in electrical burns)
  • 🔊 Cool the burn under running tap water for 20 minutes
    • Best done with assistant using timer
    • ❌ Do NOT use ice, toothpaste, gamat, or other home remedies
  • 👖 Remove tight items (jewelry, belts, shoes) from burn area
  • 🚑 Cover with clean non-adherent dressing or food-grade plastic wrap
  • ⚕️ Seek medical attention urgently

🧪 2. Burn Assessment (ABCDE Approach)

A – Airway

  • Look for signs of inhalational injury:
    • Facial burns, singed hair, hoarseness, carbon soot in mouth
  • ⚠️ Low threshold for intubation if suspected

B – Breathing

  • 100% oxygen for:
    • Burns >20% TBSA
    • Facial burns
  • Escharotomy if restrictive chest injury (circumferential full-thickness burn)

C – Circulation

  • Start IV fluids if:
    • Adults >15% TBSA
    • Children >10% TBSA
  • Check BP, pulse, CRT, bleeding

D – Disability

  • AVPU/GCS + check pupils

E – Exposure

  • Undress patient, remove jewelry
  • Log roll with spine precautions
  • Cover to avoid hypothermia

🔢 3. Burn Classification

Total Burn Surface Area (TBSA)

  • Lund & Browder chart = most accurate
  • Palm method = 1% TBSA
  • Wallace Rule of Nines (Adults)

Depth of Burn

  • ✨ Superficial: red, painful, dry, NO blisters (not counted in TBSA)
  • ☁️ Partial-thickness:
    • Superficial: pink, wet, painful, blanchable
    • Deep: blotchy red/white, delayed blanching, less painful
  • ⚪ Full-thickness: white/leathery, dry, painless, no blisters

💧 4. Fluid Resuscitation (Parkland Formula)

Indications:

  • 🏋 <12 yrs + TBSA >10%
  • 🏋 ≥12 yrs + TBSA >15%

Parkland Formula:

Adults: 4 × weight (kg) × TBSA (%) = mL in 24h (use Hartmann’s)

  • ½ in first 8h from time of injury
  • ½ in next 16h

Children <30kg:

  • 3 × weight × TBSA (Hartmann’s)
  • PLUS maintenance fluid (5% Dextrose in ½ NS)

Monitor:

  • Urine output ≥ 0.5 mL/kg/hr
  • Adjust for inhalational injury (may need more fluid)

📅 5. Referral to Burn Centre

Refer if:

  • TBSA >15% (adults), >10% (kids)
  • Full-thickness burns of any size
  • Burns on face, hands, feet, genitalia, joints
  • Circumferential burns
  • Chemical/electrical/inhalational injury
  • Suspected Non-Accidental Injury (NAI)
  • Coexisting medical conditions or trauma

🩼 6. Wound Management

Goals: Prevent infection, maintain moist healing environment

  • Assess depth frequently
  • Debride large/ruptured blisters
  • 🪠 Clean with normal saline or chlorhexidine aqueous
  • ❌ Avoid alcohol-based solutions
  • Dressing: moist occlusive non-adherent dressing
  • 💄 Face/perineum: clean with saline + topical antibiotic ointment
  • ❄ Keep patient warm, elevate limbs

SSD cream: Only use after consultation with burn team

🚗 7. Transfer Protocol

  • Use MOH Burn Transfer Checklist
  • Ensure:
    • ABC stabilization
    • Adequate analgesia
    • Fluid started
    • Wound covered
  • Document: charts, referral letter, progress notes, investigations

⚡ 8. Critical Care Considerations

Inhalational Injury

  • Suspect if facial burns, soot, hoarseness, closed space fire
  • Intubate early if airway compromise likely
  • Avoid suxamethonium after 48h (risk of hyperkalemia)

Nutrition

  • Start enteral feeding within 6-12h
  • High protein, high calorie
  • ESPEN/ASPEN guidelines followed

Pain Management

  • Avoid IM/SC
  • Use IV morphine; PCA for major burns
  • Non-opioid adjuncts: paracetamol, NSAIDs
  • Non-pharma: distraction, relaxation
  • Use FLACC, CPOT, BPS for non-verbal patients
24
Q

Pathophysiological of how Stress ulcer happened in Burn patient ( Curling ulcer)

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🔥 Pathophysiology of Stress Ulcer in Burn Patients (Curling’s Ulcer)

**1.Severe Burn Injury:**
*	Major burns (typically >30% of total body surface area) trigger a systemic inflammatory response.

**2.Hypovolemia and Splanchnic Vasoconstriction:**
*	Burn-induced hypovolemia leads to reduced plasma volume.
*	The body compensates by diverting blood away from the gastrointestinal tract (splanchnic circulation) to vital organs, causing mucosal ischemia.

**3.Mucosal Ischemia and Hypoxia:**
*	Reduced blood flow results in decreased oxygen delivery to the gastric mucosa.
*	This hypoxia impairs cellular metabolism and weakens the mucosal barrier. 

**4.Breakdown of Mucosal Defenses:**
*	Ischemia diminishes mucus and bicarbonate secretion, essential components of the gastric mucosal defense.
*	The compromised barrier allows gastric acid and pepsin to damage the mucosa.

**5.Increased Gastric Acid Secretion:**
*	Stress-related hormonal changes, including elevated gastrin levels, can increase gastric acid production, exacerbating mucosal injury.

**6.Ulcer Formation:**
*	The combined effects of mucosal ischemia, impaired defenses, and increased acid lead to mucosal erosion and ulceration, predominantly in the stomach and proximal duodenum.

**7.Potential Complications:**
*	If left untreated, Curling’s ulcers can lead to gastrointestinal bleeding, perforation, and peritonitis, significantly increasing morbidity and mortality. 

🛡️Prevention and Management

*	**Early Enteral Nutrition:**
*	Initiating feeding as soon as feasible helps maintain mucosal integrity and stimulates blood flow to the gastrointestinal tract. 

*	**Pharmacologic Prophylaxis:**
*	Administration of proton pump inhibitors (PPIs) or H2-receptor antagonists reduces gastric acid secretion, aiding in ulcer prevention.

*	**Monitoring and Supportive Care:**
*	Regular assessment for signs of gastrointestinal bleeding and prompt intervention are crucial
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Types of Branula and flow rate
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Overview of DKA
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National Early Warning Score
- National Early Warning Score was developed in 2012, through collaborative work of Royal College of Physicians (RCP) and National Health Service (NHS) Trusts in UK on the basis of there should be a national system for recognising very sick patients whose condition is deteriorating and who need more intensive medical or nursing care. - The NEWS is an adjunct to decision making, used in combination with clinical judgement and communicated across the care pathway **Standardized Communication Tool** * Provides a universal language among: * Nurses * Doctors * Paramedics * ICU teams “A NEWS of 7” means the same across all departments. **Guides Escalation of Care** * Helps staff decide when to: * Call senior clinician * Activate rapid response team * Transfer to higher care (e.g., ICU) Summary: Why NEWS Matters: ⏰ Early warning = early intervention ⚠️ Recognizes subtle deterioration 🔗 Connects teams with common scoring language 📈 Proven to reduce complications and death
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Types of Inotropes
🧪 Types of Inotropes **Positive Inotropes (Enhance cardiac contractility)** **1.Beta-Adrenergic Agonists:** * **Dobutamine:** Primarily stimulates β₁-receptors, increasing contractility with modest vasodilation. Commonly used in acute heart failure and cardiogenic shock. * **Dopamine:** Dose-dependent effects; low doses may promote renal perfusion, moderate doses enhance cardiac output via β₁-receptor stimulation, and high doses induce vasoconstriction through α-receptor activation. * **Epinephrine (Adrenaline):** Potent β₁ and α-adrenergic agonist; increases heart rate, contractility, and systemic vascular resistance. Used in cardiac arrest and anaphylactic shock.  * **Norepinephrine (Noradrenaline)**: Strong α-adrenergic effects leading to vasoconstriction; also has β₁ activity enhancing contractility. First-line agent in septic shock with hypotension. 🩺**Clinical Indications and Selection Criteria** The choice of an inotrope is guided by the patient’s hemodynamic status, underlying pathology, and specific therapeutic goals. **Cardiogenic Shock:** * **Dobutamine:** Preferred for its inotropic and vasodilatory properties, improving cardiac output. * **Norepinephrine:** Used when hypotension is profound; provides vasoconstriction and modest inotropic support. **Septic Shock:** * **Norepinephrine:** First-line agent to counteract vasodilation and maintain perfusion pressure. * **Dobutamine:** Added if myocardial dysfunction leads to low cardiac output despite adequate perfusion pressure.
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Stages of Peritonitis
Under normal circumstances, the peritoneum is a smooth serous membrane lining the abdominal cavity. Normally, this contains less than 100 ml of sterile, clear fluid with less than 3000 cells / mm3. Once this layergets inflamed, the main peritoneal defence mechanisms, or the ‘physiological’ mechanisms that come into play are: * Absorption of the purulent fluid through the diaphragmatic lymphatics. - Activation of the peritoneal mesothelial cells. * Migration of neutrophils and activation of the peritoneal macrophages. * Exudation of protein and fibrinogen rich fluid into this ‘third space’ to entrap, dilute and localize the infective fluid. The losses seen here may parallel the losses seen and estimated in patient with severe burns. Spread of the infection and transition to the stage of frank peritonitis then ensues, and this is the classical stage of peritonitis, with the patient silent and avoiding movements, with tachycardia, tachypnea and a silent abdomen with ‘board like’ rigidity and rebound.
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Define Burst abdomen
Burst abdomen refers to the **postoperative separation of the abdominal musculo-aponeurotic layers, leading to partial or complete disruption of the abdominal wall**. This separation can result in the exposure or protrusion of intra-abdominal organs through the surgical incision.
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Classification of Burst Abdomen
➔ Partial Dehiscence (⚡ skin, fat open — fascia intact) ➔ Complete Dehiscence (⚡⚡ fascia ruptured — organs at risk of coming out)
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Classification of wound
Classification of wounds Wounds may be classified by their potential for infection: - Clean wound: an operation carried out through clean, non-infected skin under sterile conditions, where the GI tract, genitourinary (GU) tract or respiratory tract are not breached, e.g. hernia repair, varicose vein surgery; risk of wound infection should be <2%. * Clean contaminated wounds: an operation carried out under sterile conditions with breaching of a hollow viscus other than the colon, where contamination is minimal, e.g. uncomplicated lap cholecystectomy, uncomplicated acute appendicitis, hysterectomy; the risk of wound infection should be <10% * Contaminated wound: an operation carried out where contamination has occurred, e.g. by opening the colon ( elective colorectal surgery), an open fracture, or animal or human bites; the risk of wound infection is around 15% -20% * Dirty wounds: an operation carried out in the presence of pus or a perforated viscus, e.g. perforated diverticulitis, perforated gallbladder empyema, perforated appendicitis with pus ,faecal peritonitis; the risk of wound infection is >40%
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🧠 CCrISP Chapter 2: Assessment of the Critically Ill Surgical Patient
🎯 **Learning Objectives** Assess critically ill patients with simultaneous resuscitation and examination Apply a systematic ABCDE approach Treat abnormal physiology immediately, even before final diagnosis Create daily management plans for both stable and unstable patients 🩺 **The Three-Stage CCrISP Assessment** 🧱 1. **Immediate Assessment – ABCDE** 🔤 A – Airway Look: Cyanosis, tracheal tug, accessory muscles, see-saw breathing Listen: Gurgling, snoring, stridor Feel: Airflow at nose/mouth Actions: High-flow oxygen via reservoir mask (12–15 L/min) Chin lift, jaw thrust, suction, airway adjuncts (Guedel, NPA) Call anaesthetist if airway unstable 🔤 B – Breathing Look: RR, cyanosis, use of muscles, chest movement Listen: Speech, wheeze, absent sounds Feel: Equal movement, tracheal shift, surgical emphysema Check: SpO₂ (note that it doesn’t detect CO₂) Actions: Sit patient up Treat reversible causes (PTX, bronchospasm, PE) Bag-mask ventilation if tiring 🔤 C – Circulation Look for shock: Cool skin, delayed CRT, tachycardia Assume hypovolaemia until proven otherwise Actions: 16G IV cannula, send bloods (FBC, U&E, Xmatch, lactate) **Fluid bolus:** - 10 mL/kg (normotensive) - 20 mL/kg (hypotensive) - 5 mL/kg (cardiac issues) Identify bleeding & escalate if surgery needed 🔤** D – Disability** Use AVPU scale: Alert / Voice / Pain / Unresponsive Common causes: hypoxia, hypotension, drugs, sepsis, hypoglycaemia Check blood glucose early 🔤 **E – Exposure** Examine full body: bleeding, wounds, rashes Preserve warmth & dignity 🔁 **Always reassess after each step.** Deterioration? Repeat ABCDE. 📝 **2. Full Patient Assessment** 📈 **Chart Review** Focus on trends, not isolated readings Review: RR, HR, BP, SpO₂, temp, UO, drain output, fluid charts 🗣️ **History & Examination** Get info from: patient, staff, notes, family Full top-to-toe exam with focus on surgical site & comorbidities 📊 **Review Results** Bloods: FBC, U&E, ABG, clotting Microbiology: Cultures Radiology: X-ray, CT, US ECG: For cardiac suspicion Use checklists to avoid missed issues 🧭 **3. Decide & Plan** 🔷 **Stable Patient** Normal observations and progressing well Make a daily plan: Labs & imaging Restart oral intake Remove unnecessary lines/drains Prescribe fluids, nutrition, VTE prophylaxis Plan physiotherapy & document clearly 🔶 **Unstable Patient** Needs urgent reassessment & further investigations (CXR, ABG, CT, etc.) Call for help: senior or ICU Document clearly: Who saw patient Interventions done Response Plan & review timing Criteria for escalation
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Chapter 12: Sepsis & Multi-Organ Failure Care of the Critically Ill Surgical Patient (CCrISP, 4th Edition)
📖 Definitions **Sepsis:** A life-threatening organ dysfunction caused by a dysregulated host response to infection. (Clinically: an increase of ≥2 points in SOFA score from baseline in response to infection.) **Septic Shock:** A subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. (Clinically: sepsis with persistent hypotension requiring vasopressors to maintain MAP ≥ 65 mmHg and serum lactate > 2 mmol/L despite adequate fluid resuscitation.) **MODS – Multi-Organ Dysfunction Syndrome:** Progressive failure of two or more organ systems in a critically ill patient, often due to uncontrolled sepsis. Indicates a high risk of death and often requires intensive care support. 🎯 **Learning Focus** - Understand sepsis as a clinical emergency requiring immediate treatment. - Prevent progression to septic shock and MODS by rapid intervention. - Manage using structured protocols such as Sepsis 6. - Emphasise source control, appropriate antibiotics, and critical care escalation. 🔬 **Pathophysiology of Sepsis** Infection triggers immune activation → cytokine surge (IL-1, IL-6, TNF-α). Leads to: Widespread vasodilation → hypotension. Capillary leakage → oedema and hypovolaemia. Microvascular thrombosis → impaired oxygen delivery. End result = tissue hypoxia, cellular dysfunction, and organ failure if untreated. ⚠️ **High-Risk Surgical Groups** - Post-abdominal or pelvic surgery patients. - Those with suspected anastomotic leaks, abscesses, or infected wounds. - Patients with central lines, urinary catheters, or surgical drains. - Immunocompromised individuals (steroids, chemotherapy, diabetes). - ICU/HDU patients with new deterioration or signs of infection. 🚨 **Clinical Recognition – Early Clues** - Fever or hypothermia. - Tachycardia, hypotension, and tachypnoea. - Confusion, restlessness, or ↓ GCS. - Oliguria or anuria. - Cool peripheries, mottled skin, prolonged capillary refill. - Elevated serum lactate = sign of tissue hypoperfusion. - Note: Elderly and immunocompromised may have atypical signs. 🛠️ **Initial Management – Sepsis 6 (within 1 hour)** - Administer high-flow oxygen to maintain SpO₂ >(92 or 88% if Chronic lung). - Take blood cultures before antibiotics. - Administer IV broad-spectrum antibiotics immediately. - Give IV fluid bolus. - Check serum lactate. - Insert urinary catheter and measure hourly output. Administer 30 ml/kg crystalloid for hypotension or lactate ≥ 4 mmol/L. These steps aim to stabilise the patient and reverse hypoperfusion. Clinical improvement must be reassessed continuously. 🏥 **If Deterioration Persists – Next Steps** - Start vasopressors (e.g. noradrenaline) if fluid resuscitation fails. Goal: Maintain MAP ≥ 65 mmHg. - **Investigate and treat source of infection:** Drain abscesses surgically or radiologically. Remove infected devices (e.g., central lines). Return to theatre if necessary (e.g., leak, peritonitis). Perform urgent CT or ultrasound to locate infection. Escalate to ICU if vasopressors or organ support are needed. 🧠 **Progression to MODS** As sepsis advances, it can affect multiple organ systems: **Lungs**: ARDS, ↓ PaO₂, need for ventilation. **Kidneys**: oliguria/anuria, rising creatinine. **Brain**: delirium, confusion, coma. **Heart**: persistent hypotension, elevated lactate. **Liver**: jaundice, ↑ LFTs, coagulopathy. **Coagulation**: thrombocytopenia, ↑ INR, DIC. **MODS** has a high mortality and must be managed in a critical care setting. ✅ **Key Takeaways** Sepsis is more than just infection — it is a dangerous systemic response. Early signs (mental status change, hypotension, oliguria) must not be missed. Complete the Sepsis 6 bundle within 1 hour of recognition. Control the infection source — antibiotics alone are not sufficient. If organs are failing or hypotension persists, escalate to ICU early. Monitor response, reassess often, and document clearly.
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how Procalcitonin helps to detect infection
⚙️ **How PCT Works in Infection:** 🔹 In Healthy People PCT is only produced in thyroid C cells, converted quickly to calcitonin. 🧪 Serum PCT level = very low. 🔥 **In Bacterial Infection / Sepsis** - Bacterial toxins (e.g. endotoxins) and cytokines (e.g. IL-1β, TNF-α, IL-6) stimulate PCT production. - Multiple organs (liver, lungs, kidneys, adipose tissue) begin to produce PCT. - Unlike thyroid production, this PCT is not converted to calcitonin → it accumulates in blood. 🟠 **PCT starts rising within 2–4 hours, peaks at 6–24 hours, and has a half-life of about 24 hours.**