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What is delirium

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delirium

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NIA delirium sudden confusion symptoms causes

Delirium is a sudden, fluctuating disturbance of brain function that causes a person to become confused and unable to focus or sustain attention. It usually develops over hours to days and can vary markedly during the day.
Typical features include:
  • Reduced attention or distractibility
  • Disorganized thinking, confusion, or altered awareness
  • Changes in alertness, from agitation to unusual sleepiness
  • Memory problems, hallucinations, or perceptual disturbances
  • A disrupted sleep-wake pattern
There are three patterns: hyperactive delirium (restless, agitated), hypoactive delirium (quiet, drowsy, withdrawn, and often missed), and mixed delirium. Hypoactive and mixed forms are particularly common and easy to overlook.
It is usually caused by an underlying acute problem, such as infection, dehydration, medication effects or withdrawal, surgery/anesthesia, low oxygen, pain, metabolic disturbance, or organ failure. Older adults and people with dementia are at higher risk.
Delirium is a medical emergency, because sudden confusion may signal a serious, treatable illness. A person with new confusion, reduced consciousness, hallucinations, or abrupt behavioral change should receive urgent medical assessment. Unlike dementia, which is generally gradual and progressive, delirium has an acute onset and fluctuates.

Paralytic ileus,diagnosis and management

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https://www.merckmanuals.com/professional/gastrointestinal-d…

Paralytic ileus

Paralytic ileus, also called adynamic ileus, is temporary failure of intestinal peristalsis without a physical blockage. The bowel becomes functionally inactive, so gas and fluid accumulate.
It commonly occurs after abdominal surgery, but may result from sepsis, peritonitis or other intra-abdominal inflammation, hypokalemia and other electrolyte abnormalities, retroperitoneal injury/hematoma, severe systemic illness, or medicines such as opioids and anticholinergics. Merck Manual review

Clinical features

  • Progressive abdominal distension
  • Nausea, vomiting, anorexia
  • Failure to pass flatus or stool, though small watery stool may occasionally pass
  • Mild, diffuse, non-colicky discomfort
  • Quiet or absent bowel sounds
  • Usually no marked localized tenderness unless the underlying cause is inflammatory or surgical
After laparotomy, temporary gut dysmotility is expected early on. Persistent or worsening symptoms should prompt assessment for a complication such as obstruction, leak, abscess, or peritonitis. Bailey and Love's Short Practice of Surgery, p. 347.

Diagnosis

Diagnosis is clinical, supported by imaging and investigation of the cause.

1. Assess and look for danger signs

Check vital signs, hydration, urine output, abdominal examination, hernias, rectal examination when appropriate, and medication history.
Features that suggest an alternative diagnosis or complication rather than uncomplicated ileus include:
  • Severe colicky pain
  • Localized tenderness, guarding, rigidity, or rebound tenderness
  • Fever, tachycardia, hypotension, or raised lactate
  • Leukocytosis or sepsis
  • Rapidly worsening distension or persistent vomiting
  • Gastrointestinal bleeding
These require urgent surgical review.

2. Laboratory tests

  • Full blood count and inflammatory markers
  • Serum electrolytes, especially potassium, magnesium, calcium, sodium
  • Urea/creatinine and glucose
  • Liver function tests if indicated
  • Serum lactate and blood cultures if bowel ischemia, perforation, or sepsis is a concern

3. Imaging

  • Plain abdominal radiograph: diffuse gaseous dilatation of both small and large bowel, often with air-fluid levels. Gas may still be visible in the rectum.
  • Contrast-enhanced CT abdomen/pelvis: preferred if diagnosis is uncertain, symptoms persist or worsen, or mechanical obstruction, ischemia, perforation, abscess, or anastomotic leak needs exclusion.
The key differential diagnosis is mechanical intestinal obstruction. CT can help identify a transition point or an underlying complication. Merck's diagnostic guidance

Management

Initial supportive management

  1. Treat the underlying cause
    • Treat sepsis, peritonitis, pneumonia, pancreatitis, or intra-abdominal pathology.
    • Correct potassium, magnesium, calcium, and fluid deficits.
    • Stop or reduce precipitating drugs, especially opioids and anticholinergic agents where possible.
  2. Bowel rest and fluid management
    • Keep nil by mouth initially if vomiting or significant distension.
    • Give IV isotonic fluids.
    • Monitor fluid balance, urine output, renal function, and electrolytes.
  3. Nasogastric tube decompression
    • Use if there is persistent vomiting, marked distension, aspiration risk, or severe discomfort.
    • It is not necessarily required in every mild postoperative ileus.
  4. Mobilize and optimize recovery
    • Encourage early mobilization where safe.
    • Use opioid-sparing analgesia where feasible.
    • Reintroduce oral intake gradually once nausea resolves, abdominal distension improves, and bowel function returns.
Supportive therapy with hydration and electrolyte correction is the usual treatment. Bailey and Love's Short Practice of Surgery, p. 347.

Persistent ileus

If prolonged, reassess actively for infection, anastomotic leak, abscess, electrolyte disturbance, medication effects, or missed mechanical obstruction. Nutritional support should be considered if enteral feeding remains impractical for a prolonged period. Bailey and Love's Short Practice of Surgery, p. 347.

Important caution on neostigmine

Neostigmine is not routine treatment for ordinary generalized postoperative paralytic ileus. It is used under monitored conditions mainly for selected cases of acute colonic pseudo-obstruction (Ogilvie syndrome) after mechanical obstruction and perforation have been excluded. It can cause bradycardia and requires appropriate monitoring.

When surgery is needed

Paralytic ileus itself is usually managed non-operatively. Surgery or urgent intervention is considered when imaging or clinical assessment identifies a cause needing source control or repair, such as:
  • Mechanical bowel obstruction
  • Perforation
  • Bowel ischemia
  • Peritonitis
  • Anastomotic leak
  • Intra-abdominal abscess
Recent systematic reviews on postoperative ileus support multimodal recovery strategies, including minimizing opioids and promoting early recovery measures, but they do not replace evaluation for surgical complications (PMIDs: 40523983, 39788451).

How to differentiate type 1 and type 2 respiratory failure with ABG

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type 1 type 2 respiratory failure PaO2 PaCO2 ABG definitions guideline

ABG differentiation

FeatureType 1 respiratory failureType 2 respiratory failure
Also calledHypoxemic respiratory failureHypercapnic or ventilatory respiratory failure
PaO₂< 60 mmHg (8 kPa)Often <60 mmHg, but may be normal if supplemental oxygen is given
PaCO₂Normal or low> 45 mmHg (6 kPa)
pHUsually normal or alkalemic earlyLow in acute disease due to respiratory acidosis
Main problemFailure of oxygenationFailure of ventilation and CO₂ elimination
Typical causesPneumonia, pulmonary edema, ARDS, pulmonary embolismCOPD exacerbation, severe asthma exhaustion, opioid/sedative effect, neuromuscular weakness, obesity hypoventilation

Easy rule

  • Type 1: low O₂ with normal/low CO₂
    PaO₂ <60 mmHg + PaCO₂ normal or low
  • Type 2: high CO₂, usually with low O₂
    PaCO₂ >45 mmHg, often with PaO₂ <60 mmHg
This agrees with the NCBI respiratory-failure review, which defines type 1 by hypoxemia with normal or decreased PaCO₂, and type 2 by hypercapnia.

Examples

Type 1

ABG on room air:
  • pH 7.47
  • PaCO₂ 32 mmHg
  • PaO₂ 52 mmHg
  • HCO₃⁻ 23 mmol/L
Interpretation: Type 1 respiratory failure. There is significant hypoxemia with low PaCO₂, often caused by tachypnea in pneumonia, pulmonary edema, or pulmonary embolism.

Acute Type 2

ABG:
  • pH 7.25
  • PaCO₂ 70 mmHg
  • PaO₂ 50 mmHg
  • HCO₃⁻ 30 mmol/L
Interpretation: Acute hypercapnic Type 2 respiratory failure, with acute respiratory acidosis.

Chronic Type 2, for example stable chronic CO₂ retention in COPD

ABG:
  • pH 7.36
  • PaCO₂ 60 mmHg
  • PaO₂ 58 mmHg
  • HCO₃⁻ 33 mmol/L
Interpretation: Chronic Type 2 respiratory failure. The raised bicarbonate indicates renal compensation for long-standing CO₂ retention.

Acute-on-chronic Type 2

ABG:
  • pH 7.22
  • PaCO₂ 85 mmHg
  • PaO₂ 48 mmHg
  • HCO₃⁻ 34 mmol/L
Interpretation: Acute-on-chronic Type 2 respiratory failure. Bicarbonate is high from chronic compensation, but the markedly low pH indicates an acute deterioration.

Exam approach to any ABG

  1. Check PaO₂: Is it <60 mmHg? If yes, hypoxemic respiratory failure is present.
  2. Check PaCO₂:
    • ≤45 mmHg: Type 1
    • 45 mmHg: Type 2
  3. Check pH and HCO₃⁻ to determine acute, chronic, or acute-on-chronic CO₂ retention.
  4. Interpret PaO₂ in relation to the FiO₂. A patient on oxygen can have a seemingly acceptable PaO₂ while still having serious gas-exchange failure.
Type 1 reflects impaired oxygen transfer, while type 2 reflects inadequate alveolar ventilation. Tintinalli's Emergency Medicine describes type 1 as hypoxia without hypercapnia and type 2 as hypoxia with hypercapnia.
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