Paracetamol poisoning

Acetaminophen poisoning

The minimum dose that causes toxicity :  In single dose – 150mg/kg  or 10gm for adult & 200mg/kg for children

Clinical features

Phase I : 30 minutes – 24 hours after ingestion

The patient may be asymptomatic or may present with anorexia, nausea, vomiting, malaise

Physical examination may reveal pallor & diaphoresis

Phase II : 18 - 72 hours after ingestion

Right upper quadrant abdominal pain , anorexia, nausea, vomiting & decreased urinary output

Physical examination may reveal upper right quadrant tenderness, tachycardia & hypotension

Phase III : 72 – 96 hours after ingestion

Also known as hepatic phase

Characterized by nausea, vomiting, abdominal pain, tender hepatic edge on palpation, jaundice, hypoglycemia, coagulopathy, hepatic encephalopathy & acute renal failure.

Death may occur due to multiorgan failure

Phase IV : 4 days – 3 weeks after ingestion

 Also known as recovery phase

Complete resolution of symptoms & recovery of organs takes place

Investigations

Plasma acetaminophen levels are measured . the values are plotted on the Rumack Matthew nomogram to determine the risk of hepatotoxicity

Liver function tests

Renal fucnction tests

PT & INR

ECG done to rule out congestion of cardioactive susbstances

Arterial blood gas – pH < 7.3 indicates poor outcome

Serum amylase & lipase levels to rule out pancreatic injury

If encephalopathy is present, CT brain is done to look for cerebral edema & arterial serum ammonia levels are obtained

Treatment

 The acute management consists of stabilizing airway, breathing & circulation & administration of the antidote- N-acetyl-Cysteine, if indicated

Indications of N-acetyl-Cysteine

Plasma acetaminophen levels above the lower line in the Rumack Matthew nomogram

Suspected ingestion ˃ 7.5gm in a single dose

Patients presenting late with laboratory evidence of liver injury & h/o acetaminophen ingestion

Patients with unknown time of ingestion with serum concentration ˃10mcg

Autosomal Recessive

Autosomal recessive

In autosomal recessive inheritance

·         only homozygotes are affected

·         males and females are equally likely to be affected

·         not manifest in every generation - may 'skip a generation'

If two heterozygote parents

·         25% chance of having an affected (homozygote) child

·         50% chance of having a carrier (heterozygote) child

·         25% chance of having an unaffected (i.e. genotypical) child

If one affected parent (i.e. homozygote for gene) and one unaffected (i.e. not a carrier or affected)

·         all the children will be carriers

Autosomal recessive disorders are often metabolic in nature and are generally more life-threatening compared to autosomal dominant conditions

Autosomal recessive conditions

Autosomal recessive conditions are often thought to be 'metabolic' as opposed to autosomal dominant conditions being 'structural', notable exceptions:

·         some 'metabolic' conditions such as Hunter's and G6PD are X-linked recessive whilst others such as hyperlipidaemia type II and hypokalaemic periodic paralysis are autosomal dominant

·         some 'structural' conditions such as ataxia telangiectasia and Friedreich's ataxia are autosomal recessive

The following conditions are autosomal recessive:

·                     Albinism

·                     Ataxia telangiectasia

·                     Congenital adrenal hyperplasia

·                     Cystic fibrosis

·                     Cystinuria

·                     Familial Mediterranean Fever

·                     Fanconi anaemia

·                     Friedreich's ataxia

·                     Glycogen storage disease

·                     Haemochromatosis

·                     Homocystinuria

·                     Lipid storage disease: Tay-Sach's, Gaucher, Niemann-Pick

·                     Mucopolysaccharidoses: Hurler's

·                     PKU

·                     Sickle cell anaemia

·                     Thalassaemias

·                     Wilson's disease

Tunnel vision

Tunnel vision is the concentric diminution of the visual fields

Causes :

• Papilloedema
• Glaucoma
• Retinitis Pigmentosa
• Choroidoretinitis
• Hysteria
• Optic atrophy secondary to tabes dorsalis