Can we give tan domeperidone to 13 year old boy

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domperidone AND children AND safety

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domperidone use in children dose contraindications age 12 years FDA EMA

Short answer: Yes, domperidone tablets can be used in a 13-year-old boy for nausea/vomiting, but only if he weighs 35 kg or more, only under medical supervision, at the lowest effective dose for the shortest time (usually not more than a week), and only after ruling out cardiac risk factors and drug interactions.

Why age 13 is on the "allowed" side of the cutoff

Following EMA and UK MHRA safety reviews, domperidone's licensed indication was narrowed:

Approved use: adults and adolescents 12 years and older, weighing 35 kg or more, for relief of nausea and vomiting.
Below 12 years or under 35 kg: no longer approved, because a randomized placebo-controlled trial in children under 12 with acute gastroenteritis showed no efficacy benefit over placebo (MHRA/GOV.UK drug safety update).

So a 13-year-old technically meets the age criterion - but the 35 kg weight threshold must also be met. If he weighs less than 35 kg, it falls outside the licensed use and an alternative should be considered with the treating doctor.

Note: in the US, domperidone is not FDA-approved at all (marketed use is essentially unavailable due to cardiac arrhythmia risk); this age/weight-based approval applies to EMA/UK/many Asian and other markets. Check what applies in your country.

Dosing (if appropriate to use)

10 mg up to 3 times daily, maximum 30 mg/day
Lowest effective dose, for the shortest duration possible (guideline default: not usually beyond ~1 week) (FAMHP flash safety update)

Before giving it, check for contraindications/cautions

Domperidone carries a boxed cardiac warning - it can cause QT prolongation, ventricular arrhythmia, and rarely sudden cardiac death, which is why its use has been restricted in Europe to short durations ("Domperidone," Yamada's Textbook of Gastroenterology, 7th ed.). Avoid or use with extra caution if the child has:

Known heart disease, arrhythmia, or prolonged QT interval
Significant electrolyte disturbances (e.g., hypokalemia)
Is on other QT-prolonging drugs or potent CYP3A4 inhibitors (azole antifungals, some macrolides like erythromycin/clarithromycin, certain antivirals) - these raise domperidone levels and arrhythmia risk, since it's metabolized via CYP3A4 (Goldman-Cecil Medicine)
Moderate-to-severe liver impairment
A prolactin-secreting pituitary tumor
GI obstruction, perforation, or active GI bleeding

Bottom line

A 13-year-old is in the approved age bracket only if he also weighs ≥35 kg, and even then domperidone should be prescribed by a doctor who has checked for cardiac risk factors and interacting medications, used at the lowest dose, and stopped once symptoms resolve (ideally within a week). This isn't a drug to self-administer or continue long-term without medical follow-up - please have his pediatrician confirm the indication, weight-based eligibility, and screen for the cautions above before giving it.

Recent literature check: a 2023 pediatric review ("Drugs in Focus: Domperidone," J Pediatr Gastroenterol Nutr, PMID 37159421) reinforces this same age/weight-restricted, short-course approach and cardiac safety caveat - consistent with the textbook and regulatory guidance above, no contradicting recent evidence found.

Iv dns infusion in alcoholic

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IV dextrose normal saline infusion alcoholic patient thiamine Wernicke risk precautions

IV DNS (Dextrose 5% in Normal Saline) in an Alcoholic Patient

The key precaution: give thiamine first (or with it), never dextrose alone

Chronic alcoholics are frequently thiamine-deficient (poor intake, malabsorption, impaired hepatic storage). Thiamine is required as a cofactor to metabolize glucose. If you infuse a dextrose-containing fluid like DNS into a thiamine-deficient patient, the sudden glucose load can precipitate or worsen Wernicke's encephalopathy - this is well documented across multiple sources (Harrison's Principles of Internal Medicine, 22nd ed.; Tintinalli's Emergency Medicine; Adams and Victor's Principles of Neurology, 12th ed.).

Practical rule: give IV thiamine 100-500 mg (IV or IM) before or concurrently with the DNS infusion - not after.

Standard prophylactic dose: 100 mg IV/IM.
If Wernicke's encephalopathy is already suspected (confusion, ataxia, ophthalmoplegia): 500 mg IV thiamine diluted in 50-100 mL saline, infused over 30 minutes, given 3 times daily for 2-3 days (Royal College of Physicians regimen), with resuscitation facilities available since rare anaphylactoid reactions can occur with IV thiamine.

Why DNS specifically is used here

DNS (5% dextrose + normal saline) is a reasonable choice in an alcoholic because it addresses several problems at once:

Volume depletion from vomiting, poor intake, or alcoholic ketoacidosis - the saline component repletes volume and sodium.
Hypoglycemia - alcoholics (especially in withdrawal, malnourished, or with alcoholic ketoacidosis) are prone to hypoglycemia because alcohol inhibits gluconeogenesis; the dextrose component treats/prevents this.
In alcoholic ketoacidosis, textbook management explicitly is "normal saline in dextrose" plus thiamine, correction of hypoglycemia, and correction of electrolytes (Goldman-Cecil Medicine; Rosen's Emergency Medicine).

Other things to check/correct alongside the infusion

Electrolytes - alcoholics are often hypokalemic, hypomagnesemic, and hypophosphatemic. Correct these, particularly before/during glucose administration, since refeeding-type shifts can worsen hypophosphatemia and hypokalemia (Washington Manual of Medical Therapeutics).
Magnesium - hypomagnesemia is common and can itself cause refractory hypokalemia and arrhythmia; consider magnesium replacement.
Glucose monitoring - check blood glucose; if genuinely in DKA-type picture (rare, distinguish from alcoholic ketoacidosis), insulin needs differ - insulin should generally not be given in pure alcoholic ketoacidosis since brisk hypoglycemia can result.
Rate/volume - avoid over-rapid correction, especially if hyponatremia is present (common in alcoholics) - rapid correction risks osmotic demyelination syndrome.
Alcohol withdrawal monitoring - watch for signs of withdrawal (tremor, autonomic instability, seizures) concurrently; benzodiazepines are the mainstay if withdrawal is emerging, separate from fluid management.

Bottom line sequence for an alcoholic needing IV DNS

Check blood glucose, electrolytes (Na, K, Mg, PO4), and clinical status first.
Give thiamine (100 mg IV/IM, or 500 mg IV if Wernicke's is suspected) before or with the start of DNS.
Start DNS at an appropriate rate for volume status; correct sodium slowly if hyponatremic.
Replace potassium, magnesium, and phosphate as needed.
Monitor for withdrawal symptoms and treat separately if they emerge.

This is standard emergency/general medicine practice for managing alcoholic patients needing dextrose-containing IV fluids, and the sequencing (thiamine before/with glucose) is the single most important safety point to remember.

A quick check of recent systematic reviews/meta-analyses on this topic did not surface anything that contradicts this standard approach - the thiamine-before-glucose practice remains the consistent recommendation across current guidelines and textbooks.

Can we give Amlodipine to head injury patient with high blood pressure

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Amlodipine in a Head Injury Patient with High BP

Short answer: Generally not the first choice for acute blood pressure control after head injury - but it isn't strictly "forbidden," and the right answer depends on whether this is an acute hypertensive crisis needing tight titration, or ongoing background hypertension in a stable/recovering patient.

Why caution is needed in the acute setting

In traumatic brain injury (TBI), blood pressure management is guided by cerebral perfusion pressure (CPP), not just the BP number in isolation. Key principles from trauma/neurocritical care guidelines:

Hypotension must be avoided - SBP should be kept above ~90-110 mmHg (Brain Trauma Foundation guidelines, 3rd/4th edition), because even brief hypotension worsens secondary brain injury.
Blood pressure is often deliberately allowed to run somewhat high to maintain CPP (CPP = MAP - ICP), especially if intracranial pressure is elevated (target CPP 50-70 mmHg per Brain Trauma Foundation; Miller's Anesthesia, 10th ed.).
When BP genuinely needs to be brought down acutely (e.g., severe hypertension risking rebleeding, or in intracerebral hemorrhage/SAH), guidelines favor short-acting, easily titratable IV agents - labetalol, nicardipine, esmolol - not oral amlodipine.

Why amlodipine specifically is a poor fit for the acute phase:

It's oral-only, with slow onset (peak effect 6-12 hours) and a very long half-life (~30-50 hours) - once given, its effect cannot be turned off or titrated if the patient becomes hypotensive or needs a lower BP target changed quickly.
In an acutely head-injured patient (reduced consciousness, risk of vomiting/aspiration, possible surgery pending, NPO status), reliable oral drug absorption is often not guaranteed.
Unpredictable/excessive BP drops are specifically dangerous in this population because hypotension reduces cerebral perfusion in a brain that's already injured and often has impaired autoregulation.

When amlodipine is reasonable

If the patient is hemodynamically stable, alert, tolerating oral intake, and has chronic essential hypertension that needs ongoing (not emergency) control - e.g., during recovery/rehabilitation phase, or if he was already on amlodipine before the injury - continuing or starting it is acceptable.
Dihydropyridine calcium channel blockers as a class are actually used deliberately in neuro-emergencies (e.g., nimodipine for aneurysmal SAH, IV nicardipine for hypertensive emergencies with brain injury), so the drug class itself is not contraindicated - it's the acute, unmonitored, non-titratable oral form that's the issue.

Practical recommendation

Acute/unstable phase: use IV, short-acting, titratable agents guided by CPP/ICP monitoring under neurosurgical/critical care direction. Avoid starting oral amlodipine here.
Stable/recovery phase with genuine chronic hypertension: amlodipine can be used as part of routine antihypertensive therapy, same as in any other patient, once the acute neuro picture is settled and oral intake is safe.
Any BP-lowering decision in a head injury patient should be made by the treating neurosurgery/critical care team with knowledge of the ICP/CT findings, not decided on BP number alone - lowering BP too far in a head injury patient can be more dangerous than the hypertension itself.

This aligns with standard neurotrauma teaching in Miller's Anesthesia, Rosen's Emergency Medicine, and Brain Trauma Foundation severe TBI guidelines - the emphasis throughout is titratable IV therapy and avoidance of hypotension, not long-acting oral agents, during the acute injury phase.

What should we infuse i

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Asking for Preferences

Your message seems to be cut off. What are you asking about infusing?

Short answer: Yes, domperidone tablets can be used in a 13-year-old boy for nausea/vomiting, but only if he weighs 35 kg or more, only under medical supervision, at the lowest effective dose for the shortest time (usually not more than a week), and only after ruling out cardiac risk factors and drug interactions.

Why age 13 is on the "allowed" side of the cutoff

Following EMA and UK MHRA safety reviews, domperidone's licensed indication was narrowed:

Approved use: adults and adolescents 12 years and older, weighing 35 kg or more, for relief of nausea and vomiting.
Below 12 years or under 35 kg: no longer approved, because a randomized placebo-controlled trial in children under 12 with acute gastroenteritis showed no efficacy benefit over placebo (MHRA/GOV.UK drug safety update).

So a 13-year-old technically meets the age criterion - but the 35 kg weight threshold must also be met. If he weighs less than 35 kg, it falls outside the licensed use and an alternative should be considered with the treating doctor.

Note: in the US, domperidone is not FDA-approved at all (marketed use is essentially unavailable due to cardiac arrhythmia risk); this age/weight-based approval applies to EMA/UK/many Asian and other markets. Check what applies in your country.

Dosing (if appropriate to use)

10 mg up to 3 times daily, maximum 30 mg/day
Lowest effective dose, for the shortest duration possible (guideline default: not usually beyond ~1 week) (FAMHP flash safety update)

Before giving it, check for contraindications/cautions

Domperidone carries a boxed cardiac warning - it can cause QT prolongation, ventricular arrhythmia, and rarely sudden cardiac death, which is why its use has been restricted in Europe to short durations ("Domperidone," Yamada's Textbook of Gastroenterology, 7th ed.). Avoid or use with extra caution if the child has:

Known heart disease, arrhythmia, or prolonged QT interval
Significant electrolyte disturbances (e.g., hypokalemia)
Is on other QT-prolonging drugs or potent CYP3A4 inhibitors (azole antifungals, some macrolides like erythromycin/clarithromycin, certain antivirals) - these raise domperidone levels and arrhythmia risk, since it's metabolized via CYP3A4 (Goldman-Cecil Medicine)
Moderate-to-severe liver impairment
A prolactin-secreting pituitary tumor
GI obstruction, perforation, or active GI bleeding

Bottom line

A 13-year-old is in the approved age bracket only if he also weighs ≥35 kg, and even then domperidone should be prescribed by a doctor who has checked for cardiac risk factors and interacting medications, used at the lowest dose, and stopped once symptoms resolve (ideally within a week). This isn't a drug to self-administer or continue long-term without medical follow-up - please have his pediatrician confirm the indication, weight-based eligibility, and screen for the cautions above before giving it.

Recent literature check: a 2023 pediatric review ("Drugs in Focus: Domperidone," J Pediatr Gastroenterol Nutr, PMID 37159421) reinforces this same age/weight-restricted, short-course approach and cardiac safety caveat - consistent with the textbook and regulatory guidance above, no contradicting recent evidence found.# IV DNS (Dextrose 5% in Normal Saline) in an Alcoholic Patient

The key precaution: give thiamine first (or with it), never dextrose alone

Chronic alcoholics are frequently thiamine-deficient (poor intake, malabsorption, impaired hepatic storage). Thiamine is required as a cofactor to metabolize glucose. If you infuse a dextrose-containing fluid like DNS into a thiamine-deficient patient, the sudden glucose load can precipitate or worsen Wernicke's encephalopathy - this is well documented across multiple sources (Harrison's Principles of Internal Medicine, 22nd ed.; Tintinalli's Emergency Medicine; Adams and Victor's Principles of Neurology, 12th ed.).

Practical rule: give IV thiamine 100-500 mg (IV or IM) before or concurrently with the DNS infusion - not after.

Standard prophylactic dose: 100 mg IV/IM.
If Wernicke's encephalopathy is already suspected (confusion, ataxia, ophthalmoplegia): 500 mg IV thiamine diluted in 50-100 mL saline, infused over 30 minutes, given 3 times daily for 2-3 days (Royal College of Physicians regimen), with resuscitation facilities available since rare anaphylactoid reactions can occur with IV thiamine.

Why DNS specifically is used here

DNS (5% dextrose + normal saline) is a reasonable choice in an alcoholic because it addresses several problems at once:

Volume depletion from vomiting, poor intake, or alcoholic ketoacidosis - the saline component repletes volume and sodium.
Hypoglycemia - alcoholics (especially in withdrawal, malnourished, or with alcoholic ketoacidosis) are prone to hypoglycemia because alcohol inhibits gluconeogenesis; the dextrose component treats/prevents this.
In alcoholic ketoacidosis, textbook management explicitly is "normal saline in dextrose" plus thiamine, correction of hypoglycemia, and correction of electrolytes (Goldman-Cecil Medicine; Rosen's Emergency Medicine).

Other things to check/correct alongside the infusion

Electrolytes - alcoholics are often hypokalemic, hypomagnesemic, and hypophosphatemic. Correct these, particularly before/during glucose administration, since refeeding-type shifts can worsen hypophosphatemia and hypokalemia (Washington Manual of Medical Therapeutics).
Magnesium - hypomagnesemia is common and can itself cause refractory hypokalemia and arrhythmia; consider magnesium replacement.
Glucose monitoring - check blood glucose; if genuinely in DKA-type picture (rare, distinguish from alcoholic ketoacidosis), insulin needs differ - insulin should generally not be given in pure alcoholic ketoacidosis since brisk hypoglycemia can result.
Rate/volume - avoid over-rapid correction, especially if hyponatremia is present (common in alcoholics) - rapid correction risks osmotic demyelination syndrome.
Alcohol withdrawal monitoring - watch for signs of withdrawal (tremor, autonomic instability, seizures) concurrently; benzodiazepines are the mainstay if withdrawal is emerging, separate from fluid management.

Bottom line sequence for an alcoholic needing IV DNS

Check blood glucose, electrolytes (Na, K, Mg, PO4), and clinical status first.
Give thiamine (100 mg IV/IM, or 500 mg IV if Wernicke's is suspected) before or with the start of DNS.
Start DNS at an appropriate rate for volume status; correct sodium slowly if hyponatremic.
Replace potassium, magnesium, and phosphate as needed.
Monitor for withdrawal symptoms and treat separately if they emerge.

This is standard emergency/general medicine practice for managing alcoholic patients needing dextrose-containing IV fluids, and the sequencing (thiamine before/with glucose) is the single most important safety point to remember.

A quick check of recent systematic reviews/meta-analyses on this topic did not surface anything that contradicts this standard approach - the thiamine-before-glucose practice remains the consistent recommendation across current guidelines and textbooks.# Amlodipine in a Head Injury Patient with High BP

Short answer: Generally not the first choice for acute blood pressure control after head injury - but it isn't strictly "forbidden," and the right answer depends on whether this is an acute hypertensive crisis needing tight titration, or ongoing background hypertension in a stable/recovering patient.

Why caution is needed in the acute setting

In traumatic brain injury (TBI), blood pressure management is guided by cerebral perfusion pressure (CPP), not just the BP number in isolation. Key principles from trauma/neurocritical care guidelines:

Hypotension must be avoided - SBP should be kept above ~90-110 mmHg (Brain Trauma Foundation guidelines, 3rd/4th edition), because even brief hypotension worsens secondary brain injury.
Blood pressure is often deliberately allowed to run somewhat high to maintain CPP (CPP = MAP - ICP), especially if intracranial pressure is elevated (target CPP 50-70 mmHg per Brain Trauma Foundation; Miller's Anesthesia, 10th ed.).
When BP genuinely needs to be brought down acutely (e.g., severe hypertension risking rebleeding, or in intracerebral hemorrhage/SAH), guidelines favor short-acting, easily titratable IV agents - labetalol, nicardipine, esmolol - not oral amlodipine.

Why amlodipine specifically is a poor fit for the acute phase:

It's oral-only, with slow onset (peak effect 6-12 hours) and a very long half-life (~30-50 hours) - once given, its effect cannot be turned off or titrated if the patient becomes hypotensive or needs a lower BP target changed quickly.
In an acutely head-injured patient (reduced consciousness, risk of vomiting/aspiration, possible surgery pending, NPO status), reliable oral drug absorption is often not guaranteed.
Unpredictable/excessive BP drops are specifically dangerous in this population because hypotension reduces cerebral perfusion in a brain that's already injured and often has impaired autoregulation.

When amlodipine is reasonable

If the patient is hemodynamically stable, alert, tolerating oral intake, and has chronic essential hypertension that needs ongoing (not emergency) control - e.g., during recovery/rehabilitation phase, or if he was already on amlodipine before the injury - continuing or starting it is acceptable.
Dihydropyridine calcium channel blockers as a class are actually used deliberately in neuro-emergencies (e.g., nimodipine for aneurysmal SAH, IV nicardipine for hypertensive emergencies with brain injury), so the drug class itself is not contraindicated - it's the acute, unmonitored, non-titratable oral form that's the issue.

Practical recommendation

Acute/unstable phase: use IV, short-acting, titratable agents guided by CPP/ICP monitoring under neurosurgical/critical care direction. Avoid starting oral amlodipine here.
Stable/recovery phase with genuine chronic hypertension: amlodipine can be used as part of routine antihypertensive therapy, same as in any other patient, once the acute neuro picture is settled and oral intake is safe.
Any BP-lowering decision in a head injury patient should be made by the treating neurosurgery/critical care team with knowledge of the ICP/CT findings, not decided on BP number alone - lowering BP too far in a head injury patient can be more dangerous than the hypertension itself.

This aligns with standard neurotrauma teaching in Miller's Anesthesia, Rosen's Emergency Medicine, and Brain Trauma Foundation severe TBI guidelines - the emphasis throughout is titratable IV therapy and avoidance of hypotension, not long-acting oral agents, during the acute injury phase.Your message looks like it got cut off - could you finish the question? For example, are you asking:

What should i infuse iv to stop vomiting

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IV antiemetic drugs for vomiting ondansetron metoclopramide dose adults

IV Antiemetics to Stop Vomiting

The choice depends on the cause, but here are the standard first-line IV options used in adults:

First-line: Ondansetron (5-HT3 antagonist)

Dose: 4-8 mg IV, given over 2-5 minutes (diluted); can repeat/continue at 4-8 mg IV every 8 hours if needed.
Preferred as first-line for undifferentiated nausea/vomiting because of a favorable side-effect profile - it's not sedating and doesn't cause the dystonic reactions metoclopramide can (Rosen's Emergency Medicine; Roberts and Hedges' Clinical Procedures in Emergency Medicine).
Watch for: QT prolongation - use caution with other QT-prolonging drugs or electrolyte disturbances (hypokalemia/hypomagnesemia).

Second-line / add-on: Metoclopramide (dopamine antagonist, prokinetic)

Dose: 10 mg IV, may repeat once after 30 minutes if inadequate response.
Useful especially when there's a gastric-emptying/prokinetic component (e.g., gastroparesis, gastritis).
Can cause acute dystonia/akathisia (facial or tongue spasm, restlessness) - if this occurs, treat with diphenhydramine 25 mg IV.
Avoid in suspected bowel obstruction or Parkinson's disease.

If both above fail: Droperidol or Haloperidol

Low-dose droperidol or haloperidol can be used as rescue therapy in patients at low risk of QT-related adverse effects, when mechanical obstruction is unlikely (Rosen's Emergency Medicine).

Other situational options

Promethazine or dimenhydrinate - useful rescue agents, but more sedating.
Dexamethasone IV - often combined with ondansetron, especially for postoperative or chemotherapy-induced nausea/vomiting.
Pyridoxine + doxylamine - first-line specifically for nausea/vomiting of pregnancy (not for general use).

Practical first choice

For most adults with vomiting of unclear or non-obstructive cause (gastroenteritis, alcoholic gastritis, post-op, etc.): Ondansetron 4-8 mg IV is the reasonable first-line infusion, with metoclopramide 10 mg IV as the next step if vomiting continues.

Important - treat the underlying cause too

IV antiemetics control the symptom, but you still need to identify why the patient is vomiting (e.g., alcoholic gastritis/ketoacidosis, raised intracranial pressure from head injury, bowel obstruction, medication effect) since some causes need specific treatment beyond antiemetics - and in a head-injury patient, persistent vomiting can itself be a red flag for raised ICP that needs urgent neuro-imaging rather than just antiemetic control.

If this question relates to one of the patients you mentioned earlier (the alcoholic patient or the head-injury patient), let me know and I can tailor the antiemetic choice and fluid pairing (e.g., with thiamine/DNS, or avoiding sedating agents that mask neuro exam) specifically to that context.