palliative symptom management

Receptor-targeted antiemetics, dyspnoea management, terminal secretions, delirium assessment and phased pharmacotherapy, malignant bowel obstruction, and cachexia.

dyspnoea

non-pharmacological: upright positioning ≥45°, cool room, handheld fan directed at trigeminal area
opioid-naive: morphine 2.5 mg PO q6h + 1 mg PO q2h PRN
already on opioids: increase baseline dose by 30%
supplemental O₂ only if hypoxaemic (PaO₂ <7.3 kPa / SpO₂ ≤88%) — no benefit if normoxaemic

terminal secretions vs aspiration

distinguish before treating

Aspiration (PPS 20–30%, intact cough reflex, coughing after intake): antimuscarinics will not clear aspirate — support with comfort feeding, positioning, not glycopyrrolate. True death rattle (PPS 10–20%, depressed pharyngeal reflex, unconscious gurgling): pooled upper airway mucus → treat with antimuscarinics below.

positioning: HOB ≥30°, roll pillow under shoulder, head turned slightly to side with chin inclined downward
avoid deep suctioning; gentle oropharyngeal clearance only
antimuscarinics:
- glycopyrrolate 0.2–0.4 mg SC q4h PRN (or standing ATC)
- hyoscine hydrobromide (scopolamine) 0.2–0.4 mg SC q2–4h PRN
- atropine 1% ophthalmic drops 1–2 drops SL q4h PRN

intractable hiccups (>48h)

etiology-driven: metoclopramide (gastric distention), PPIs (GORD), dexamethasone (raised ICP)
symptomatic: chlorpromazine 25–50 mg PO TID–QID, baclofen 5–10 mg PO TID–QID, haloperidol 1–2.5 mg PO/SC q4h PRN

intractable cough

opioid antitussives: codeine 15–30 mg PO TID–QID or dextromethorphan 10–20 mg PO q4–6h
nebulised lidocaine 2% (2.5–5 mL TID–QID; hold PO intake post-nebulisation) or nebulised sodium cromoglycate

delirium

screening and workup

screen: NuDESC ≥2 triggers formal assessment, or CAM
reversible causes: hypercalcaemia, urinary retention, faecal impaction, hypoxia, CNS metastases, opioid neurotoxicity

phased management

Severity	Options
mild	non-pharmacological reorientation preferred; if needed — haloperidol 0.25–0.5 mg PO/SC q1h PRN, quetiapine 12.5–25 mg PO, olanzapine 2.5 mg PO
moderate	haloperidol 1–2 mg SC q4h PRN/standing (minimal sedation — preserves interactive time with family), or methotrimeprazine 5–12.5 mg SC q6–8h (multi-receptor, highly sedating — reserve for when awake time no longer prioritised)
severe / crisis	midazolam 1–5 mg SC q30min PRN ± methotrimeprazine 12.5–25 mg SC q30min PRN → transition to regular q6h ATC; consider continuous SC midazolam if palliative sedation criteria met

antipsychotics at end of life

Routine antipsychotic use does not alleviate end-of-life distress and may worsen motor adverse effects. Reserve for hyperactive delirium with clear distress.

Parkinson’s disease

Avoid haloperidol and metoclopramide — D₂ antagonism precipitates acute motor crises, akathisia. Use quetiapine if antipsychotic strictly needed. Never abruptly stop levodopa–carbidopa → risk of parkinsonism-hyperpyrexia syndrome (NMS-like: rigidity, hyperthermia, autonomic instability). Taper dopaminergics gradually.

nausea and vomiting — receptor-targeted selection

receptor–site map

Site	Receptors	Agents
CTZ	D₂, 5-HT₃, NK₁	haloperidol, ondansetron, aprepitant
vomiting centre	H₁, M₁, 5-HT₃	dimenhydrinate, hyoscine, ondansetron
vestibular	H₁, M₁	dimenhydrinate, hyoscine hydrobromide
GI tract	5-HT₃, D₂	ondansetron, metoclopramide
cortex / limbic	GABA	lorazepam (anticipatory nausea)

by mechanism

Mechanism	Agents
opioid-induced / gastroparesis	metoclopramide 10–15 mg PO/SC TID–QID (prokinetic/D₂), domperidone 10 mg PO TID, haloperidol 0.5–1 mg PO/SC (central D₂)
chemotherapy / radiation	5-HT₃ antagonists (ondansetron 4–8 mg TID, granisetron 1–2 mg OD) ± dexamethasone 4–8 mg OD–TID
vestibular	dimenhydrinate 25–50 mg PO/SC/IV TID–QID, hyoscine hydrobromide
bowel obstruction	see MBO section below — avoid prokinetics if complete
broad-spectrum / refractory	methotrimeprazine or olanzapine (D₂ + 5-HT₂/₃ + H₁ + M₁)

5-HT₃ antagonists are highly constipating — use cautiously if opioid-induced constipation is contributing. If single-agent therapy fails, combine agents targeting distinct receptor pathways.

malignant bowel obstruction (inoperable)

complete mechanical obstruction

discontinue prokinetics and oral laxatives
haloperidol 1–2 mg SC BID–TID (nausea)
octreotide 100–200 µg SC BID–TID or CSCI 300–600 µg/day (reduces intraluminal secretions)
hyoscine butylbromide 10–20 mg SC TID–QID or CSCI 60–90 mg/day (colic)
dexamethasone 4–10 mg SC/IV OD–TID (peritumoral oedema)

partial / functional obstruction

metoclopramide SC/CSCI (60–120 mg/day) may be continued

constipation

prevention: senna 1–2 tabs OD (up to 9/day) + lactulose 15–30 mL OD (or PEG 17 g in 250 mL water)
opioid-induced, refractory: methylnaltrexone SC (8 mg for 38–61 kg; 12 mg for 62–114 kg)

malignant ascites

therapeutic paracentesis: 4–6 L via gravity over 60–120 min (safe without albumin replacement in malignant ascites)
reserve spironolactone/furosemide for secondary portal hypertension or cirrhosis

anorexia-cachexia syndrome

dexamethasone 4–6 mg PO OD or megestrol acetate 80–160 mg PO up to TID
enteral/parenteral nutrition does not improve survival in end-stage cachexia → counsel families explicitly
comfort feeding: in advanced dysphagia, support patient-directed oral intake (purees, ice cream, thickened fluids) rather than tube feeding; follow patient’s hunger/satiety cues, do not force-feed

end-of-life glycaemic management

goal shifts to preventing symptomatic hypo (<4 mmol/L) or symptomatic hyper (>18–20 mmol/L causing polyuria, dehydration, delirium) — not tight microvascular targets
permissive range: 8–15 mmol/L; generally withhold intervention until glucose >18–20 mmol/L
type 2 DM: discontinue or drastically reduce basal insulin with declining intake; use low-dose short-acting insulin PRN for symptomatic elevations; if stable <15 mmol/L with minimal intake → stop all monitoring and insulin
type 1 DM: retain low-dose basal insulin to prevent DKA, but liberalise targets