Medicine — Infectious Diseases, NMC MBBS licence examination syllabus (Nepal Medical Council).
Sepsis: when the response becomes the disease
The infection starts it. What kills the patient is what the body does next.
Most infections are handled locally and quietly. Sepsis is what happens when that response stops being proportionate — when the inflammatory cascade meant to contain an infection instead dilates vessels everywhere, leaks fluid out of the circulation, activates coagulation and starves organs of oxygen.
The clinically important consequence is that sepsis is defined by organ dysfunction, not by how ill the infection looks. A patient with a urinary infection who becomes confused has sepsis. A patient with florid cellulitis, a fever of 39.5°C and entirely normal organ function does not. Getting that boundary right decides who needs an hour of urgent work and who needs oral antibiotics and a review.
🩺 Where this lives: The commonest way sepsis is missed is by waiting for a fever. An 84-year-old with a urinary source may present with nothing but new confusion and a temperature of 36.1°C — and hypothermia in infection carries a worse prognosis than fever, because it usually means the response is failing rather than absent. "No fever, so probably not infection" is the sentence that precedes a preventable death, and it is repeated on ward rounds daily.
The spectrum, and where the line sits
Notice that septic shock is defined by what happens after fluid, not by the initial blood pressure. A patient whose pressure recovers with a fluid bolus has sepsis; a patient still requiring vasopressors to maintain perfusion despite adequate resuscitation has septic shock, and a substantially higher mortality. That is why the definition is written around the response to treatment rather than a single reading.
RECOGNISING ORGAN DYSFUNCTION AT THE BEDSIDE
BRAIN new confusion, drowsiness, agitation —
often the FIRST sign in the elderly
CIRCULATION hypotension, prolonged capillary refill,
raised lactate
KIDNEY falling urine output, rising creatinine
LUNG hypoxia, rising oxygen requirement,
tachypnoea
LIVER rising bilirubin
CLOTTING falling platelets, deranged clotting
Scoring systems exist and are useful, but the reasoning
is the same in every one: does this patient with an
infection have an organ that is no longer working
properly? If yes, that is sepsis.
Who is at risk
🔍 The groups in whom suspicion should be lowest to trigger
Extremes of ageThe very young and the elderly, in whom presentation is atypical and physiological reserve is limited.
ImmunosuppressedChemotherapy, corticosteroids, biologics, HIV, asplenia. Neutropenic sepsis is a medical emergency — a fever in a patient on chemotherapy warrants immediate antibiotics, before the source is known and before the count returns.
Chronic diseaseDiabetes, chronic kidney or liver disease, malnutrition.
Breached barriersRecent surgery, indwelling lines and catheters, burns, intravenous drug use.
Pregnancy and the postpartum periodPhysiological changes mask deterioration, and sepsis remains a major cause of maternal death.
AspleniaParticular risk from encapsulated organisms — pneumococcus, meningococcus, Haemophilus — which is why these patients are vaccinated and often carry standby antibiotics.
The first hour
💡 Exam angle: the sequencing question is asked in several disguises, and the answer is always the same. Take cultures before antibiotics — but never delay antibiotics to obtain them. Mortality in septic shock rises measurably with each hour of delay to effective antimicrobial therapy. If venous access is difficult, or imaging would take an hour, the antibiotic goes in first. A question offering "wait for the CT before starting antibiotics" is testing exactly this.
CHOOSING THE ANTIBIOTIC
Start BROAD, based on:
the likely SOURCE and its usual organisms
whether the infection is COMMUNITY or HOSPITAL acquired
recent antibiotics, known colonisation, allergies
LOCAL resistance patterns and guidelines
Then DE-ESCALATE when cultures return — narrow the
spectrum, stop what is unnecessary, set a stop date.
This step is routinely forgotten and is where
antimicrobial resistance is generated. (The antibiotics
chapter makes the same argument from the microbe's side.)
ROUTE: intravenous in sepsis. Absorption from the gut is
unreliable in a shocked patient.
Where is the source?
Source control is not optional. No antibiotic sterilises undrained pus, an obstructed and infected kidney, a perforated viscus or an infected prosthetic line. A patient who fails to improve on appropriate antibiotics usually has a collection that needs draining, an obstruction that needs relieving, or a device that needs removing — and the answer is a procedure rather than a broader drug.
Why the shocked septic patient is warm
💡 Exam angle: this connects directly to the shock chapter. Septic shock is distributive — low systemic vascular resistance with a normal or high cardiac output — so the patient is warm and flushed with a bounding pulse and wide pulse pressure, unlike the cold, clamped-down patient in hypovolaemic or cardiogenic shock. Questions frequently give the peripheral findings and expect you to name the category, then choose fluid and a vasopressor rather than the treatments appropriate to a cold shock.
Investigations and monitoring
WHAT TO SEND, AND WHY
BLOOD CULTURES ideally two sets, before
antibiotics; from any line as well
as peripherally if a line source
is suspected
FULL BLOOD COUNT raised or LOW white count — both
abnormal; low platelets suggest
severity
UREA AND CREATININE renal dysfunction
LIVER FUNCTION hepatic dysfunction
CLOTTING disseminated intravascular
coagulation
CRP / procalcitonin support the picture; neither
diagnoses nor excludes sepsis alone
LACTATE tissue perfusion — a raised lactate
can be the only abnormal number in
a normotensive patient
BLOOD GAS the metabolic acidosis of
hypoperfusion, with respiratory
compensation (see the acid-base
chapter)
IMAGING AND SITE-SPECIFIC SAMPLES
urine, sputum, CSF, wound swabs,
aspirated pus — guided by the
suspected source
REASSESS CONTINUOUSLY. Sepsis is a moving target, and a
patient who looked stable an hour ago may not be.
Complications
MULTI-ORGAN DYSFUNCTION
The common final pathway, and the usual cause of death.
DISSEMINATED INTRAVASCULAR COAGULATION
Widespread activation of coagulation consumes platelets
and clotting factors → simultaneous THROMBOSIS and
BLEEDING. Falling platelets with rising D-dimer and
prolonged clotting.
ACUTE KIDNEY INJURY
Sepsis is the commonest cause of AKI in hospital.
ACUTE RESPIRATORY DISTRESS SYNDROME
Non-cardiogenic pulmonary oedema with refractory hypoxia.
CRITICAL ILLNESS COMPLICATIONS
Weakness, delirium, venous thromboembolism, pressure
injury, and a long recovery afterwards that is easy to
underestimate.
Clinical reasoning: four presentations
🔍 Case 1 — the missing fever
PresentationAn 84-year-old care home resident is newly confused. Temperature 35.8°C, pulse 104, BP 104/58, creatinine risen from 90 to 168, lactate 3.2. Urine dipstick positive.
The distractorNo fever, so infection seems unlikely.
ReasoningNew confusion, renal impairment and a raised lactate are organ dysfunction. With a probable urinary source, this is sepsis regardless of temperature — and hypothermia is a poor prognostic sign rather than evidence against infection.
AnswerTreat as sepsis now: cultures, lactate, urine output, oxygen if hypoxic, intravenous antibiotics and fluid, all within the hour. Do not wait for a fever that may never come.
🔍 Case 2 — the delayed antibiotic
PresentationA patient with suspected intra-abdominal sepsis, BP 84/50 and lactate 4.8. The team plans a CT to identify the source before choosing an antibiotic. The scanner is 45 minutes away.
TrapWanting the diagnosis before committing to treatment.
ReasoningMortality in septic shock rises with each hour of delay to effective antibiotics. Broad-spectrum cover appropriate to the suspected source can be started now and narrowed later; the CT informs source control, not whether to treat.
AnswerCultures, then antibiotics immediately, fluid resuscitation, and the CT in parallel. Imaging never delays the first dose.
🔍 Case 3 — the antibiotic that is not enough
PresentationA patient with pyelonephritis and an obstructing ureteric stone has had 48 hours of appropriate intravenous antibiotics but remains febrile, hypotensive and oliguric.
Key clueCorrect antibiotic, no improvement — something is not being reached.
ReasoningAn infected, obstructed urinary system is a closed collection of pus. Antibiotics cannot sterilise it while the obstruction persists, and the patient will continue to deteriorate.
AnswerUrgent decompression — nephrostomy or stent. This is source control, and it is the treatment. Broadening the antibiotic instead would be treating the wrong problem.
🔍 Case 4 — the normal blood pressure
PresentationA 46-year-old with pneumonia: BP 118/74, pulse 112, respiratory rate 26, warm peripheries, mildly confused, lactate 4.1.
The distractorA normal blood pressure suggesting the patient is not shocked.
ReasoningThe raised lactate signals tissue hypoperfusion despite a maintained pressure — compensation is holding the number up. Confusion is organ dysfunction. Warm peripheries fit distributive physiology.
AnswerThis is sepsis with hypoperfusion, and it warrants full urgent treatment. As in the shock chapter, waiting for hypotension means waiting for compensation to fail — which happens abruptly.
Commonly confused
Confusion
The distinction
Why it matters
Infection vs sepsis
Sepsis requires organ dysfunction
Decides who needs an urgent hour of work.
Sepsis vs septic shock
Shock persists despite adequate fluid
Defines escalation to vasopressors and critical care.
No fever vs no infection
Elderly and severe cases may be hypothermic
Hypothermia is a worse sign than fever.
Normal BP vs adequate perfusion
Lactate can be raised with a normal pressure
Compensation holds the number up until it fails.
Cultures first vs antibiotics first
Take cultures, but never delay antibiotics
Mortality rises with every hour of delay.
Broader antibiotic vs source control
Undrained pus needs a procedure
Failure to respond usually means an uncontrolled source.
Septic vs cardiogenic shock
Septic is warm with low SVR; cardiogenic is cold
Fluid helps one and harms the other.
Rapid revision
MUST-KNOW FACTS
1. Sepsis = infection PLUS organ dysfunction.
2. Septic shock = circulatory failure persisting DESPITE adequate fluid.
3. Sepsis is the dysregulated RESPONSE, not simply a severe infection.
4. Fever is not required; hypothermia is a WORSE prognostic sign.
5. New confusion is often the first sign in the elderly.
6. Organ dysfunction: brain, circulation, kidney, lung, liver, clotting.
7. Take blood cultures — but NEVER delay antibiotics to get them.
8. Mortality rises with each hour of delay to effective antibiotics.
9. First hour: take cultures, lactate, urine output; give oxygen,
antibiotics, fluid.
10. Antibiotics and source control cure; fluid supports.
11. Start broad, then DE-ESCALATE when cultures return.
12. Give antibiotics intravenously — gut absorption is unreliable in shock.
13. Source control is not optional: drain pus, relieve obstruction,
remove infected devices.
14. Failure to improve on correct antibiotics suggests an uncontrolled source.
15. Septic shock is DISTRIBUTIVE — warm, low SVR, high output.
16. A raised lactate can be the only abnormality in a normotensive patient.
17. Neutropenic sepsis is an emergency — antibiotics immediately.
18. Asplenic patients are at risk from encapsulated organisms.
19. Sepsis is the commonest hospital cause of acute kidney injury.
20. DIC: falling platelets, prolonged clotting, thrombosis AND bleeding.
21. CRP and procalcitonin support the picture but neither rules sepsis in or out.
22. Look for the source everywhere — including lines, the back and the perineum.
23. Reassess continuously; sepsis is a moving target.
💡 Exam angle: the reliable threads are (a) organ dysfunction defining sepsis rather than severity of infection, (b) the absent fever in an elderly patient, (c) antibiotics before imaging, (d) source control when antibiotics alone fail, and (e) the warm shock pattern. This chapter deliberately overlaps shock, antibiotics and acid–base — sepsis is where those three meet, and questions often test the junction rather than any one of them.
Syllabus points
Infection, sepsis and septic shock: where the lines sit
Recognising organ dysfunction at the bedside
Why fever is not required and hypothermia is worse
Patients at particular risk, including neutropenia and asplenia
The first hour: what to take and what to give
Antibiotic choice, route and de-escalation
Finding the source
Source control and why antibiotics alone can fail
Why septic shock is warm: distributive physiology
Investigations and the role of lactate
Complications including DIC and ARDS
Create a free account to tick topics off, take notes as you read, watch the video lessons and get a day-by-day study plan built around your exam date.