Management acute gastro bleed (part 2)

CVP line:
Consider for high risk patients eg increasing age, CV disease, on B-blockers.

Acute drug therapy:
Following successful endoscopic therapy in patients with major ulcer bleeding, IV omeprazole (80mg stat followed by 8mg/h for 72h) is recommended.
There is no firm evidence to support the use of somatostatin or antifibrinolytic therapy in the majority of patients.

Variceal bleeding:
Resuscitate then proceed to urgent endoscopy for banding or sclerotherapy. Give octreotide 50µg/h IVI for 2-5d. Terlipressin may also be used.
If massive bleed or bleeding continues, pass a Sengstaken-Blakemore tube.
A bleed is the equivalent of a large protein meal so start treatment to avoid hepatic encephalopathy.
Esomeprazole 40mg PO may also be helpful in preventing stress ulceration.

Endoscopy:
Within 4h if you suspect variceal bleeding;
within 12-24h if shocked on admission or significant comorbidity.
Endoscopy can identify the site of bleeding, estimate the risk of rebleeding and can be used to administer treatment.

No site of bleeding identified:
Bleeding site missed on endoscopy; bleeding site has healed (Mallory-Weiss tear or Dieulafoy's lesion); nose bleed (swallowed blood); site distal to 3rd part of the duodenum (Meckel's diverticulum, colonic site).

Rebleeds
Serious event: 40% of patients who rebleed will die. If "˜ at risk" maintain a high index of suspicion.
If a rebleed occurs, check vital signs every 15min and call senior cover.
To prevent rebleeding in endoscopically-proven high risk cases, IVI omeprazole has been tried, eg 80mg followed by an infusion of 8mg/h for 72h, then 20mg/24h PO for 8wks.

Signs of a rebleed:
Rising pulse rate.
Falling JVP decreasing hourly urine output.
Haematemesis or melaena.
Fall in BP (a late and sinister finding) and decreased conscious level.

Management :Acute upper gastrointestinal bleeding

Management:

Is the patient shocked?
Cool & clammy to touch (especially nose, toes, fingers) ↓capillary refill.
Pulse >100bpm.
JVP <1cm H2O.
Systolic BP <100mmHg.
Postural drop (>20mmHg on standing).
Urine output <30mL/h.

If not shocked:
Insert 2 big cannulae; start slow saline IVI to keep lines patent; check bloods and monitor vital signs + urine output.
Aim to keep Hb >8g/dL.
NB: Hb may not fall until circulating volume is restored.

If shocked:

Acute upper gastrointestinal bleeding

Acute upper gastrointestinal bleeding

Causes
Peptic ulcer ~40%.
Mallory Weiss tear 15%.
Gastroduodenal erosions ~10%.
Oesophagitis ~10%.
Varices ~7%.

Other: malignancy, vascular malformations, haemoptysis (swallowed blood).

Signs & symptoms
Haematemesis, or melaena, dizziness (especially postural),
fainting, abdominal pain, dysphagia?
Postural hypotension, hypotension, tachycardia (not if on B-blocker),
increase JVP, increase urine output,
cool and clammy, signs of chronic liver disease;
telangiectasia or purpura;
jaundice (biliary colic + jaundice + melaena suggests haemobilia).
NB: ask about previous GI problems, drug use, and alcohol intake.

Management of Pulmonary Embolism

Management

Try to prevent further thrombosis with compression stockings.
Heparin concurrently with warfarin for 5d, and until INR >2. Then stop.

If obvious remedial cause, 6wks' treatment with warfarin may be sufficient.
Otherwise, continue for at least 3-6 months (long-term if recurrent emboli, or underlying malignancy).

Is there an underlying cause, eg thrombophilic tendency, malignancy (especially prostate, breast, or pelvic cancer), SLE, or polycythaemia?

If good story and signs, make the diagnosis.

Start treatment before definitive investigations: most PE deaths occur within 1h.

PE : Signs and symptoms

Signs and symptoms
Acute dyspnoea, pleuritic chest pain, haemoptysis, and syncope.
Hypotension, tachycardia, gallop rhythm, JVP up, loud P2, right ventricular heave, pleural rub, tachypnoea, and cyanosis, AF.
Classically, PE presents 10d post-op, with collapse and sudden breathlessness while straining at stool—but PE may occur after any period of immobility, or with no predisposing factors. Breathlessness may be the only sign. Multiple small emboli may present less dramatically with pleuritic pain, haemoptysis, and gradually increasing breathlessness.
Look for a source of emboli—especially DVT (is a leg swollen?).

Investigations
U&E, FBC, baseline clotting.
ECG (commonly normal or sinus tachycardia); right ventricular strain pattern V1-3), right axis deviation, RBBB, AF, may be deep S-waves in I, Q-waves in III, inverted T-waves in III (˜SI QIII TIII).
CXR often normal; decreased vascular markings, small pleural effusion. Wedge-shaped area of infarction. Atelectasis.
ABG: hyperventilation + gas exchange: PaO2, PaCO2, pH often.
CT pulmonary angiography is sensitive and specific in determining if emboli are in pulmonary arteries. If helical CT is unavailable, a ventilation-perfusion ([V with dot above]/[Q with dot above]) scan can aid diagnosis. If [V with dot above]/[Q with dot above] scan is equivocal, pulmonary angiography or bilateral venograms may help (MRI venography or plethysmography are alternatives).
D-dimer blood test, if thrombosis present. May help in excluding a PE.

Massive pulmonary embolism (PE)

Massive pulmonary embolism (PE)
Always suspect pulmonary embolism (PE) in sudden collapse 1-2wks after surgery. Death rate in England and Wales: 30,000-40,000/yr.
Mechanism
Venous thrombi, usually from DVT, pass into the pulmonary circulation and block blood flow to lungs. The source is often occult.

Risk factors
Malignancy.
Surgery especially pelvic.
Immobility.
The Pill (there is also a slight risk attached to HRT).
Previous thromboembolism and inherited thrombophilia.

Prevention
Early post-op mobilization is the simplest method; consider:
Antithromboembolic (TED) stockings.
Low molecular weight heparin prophylaxis SC.
Avoid contraceptive pill if at risk, eg major or orthopaedic surgery.
Recurrent PEs may be prevented by anticoagulation, vena caval filters are of limited use, and should be combined with anticoagulation.

Antibiotic treatment of pneumonia