Tetanus

- Is a potentially lethal condition characterised by muscular rigidity and spasms, caused by the tetanospasmin toxin produced by Clostridium tetani

Types:

• cephalic
• local
• generalised
• neonatal (50% of tetanus deaths worldwide)

Tetanospasmin

• taken up by motor nerves or haematogenous spread to CNS
• preferentially prevents discharge from GABA inhibitory interneurons in spinal cord and brainstem -> unrestricted motor nerve activity and autonomic instability

Clinical features:

Clinical triad of rigidity, muscle spasms and, autonomic dysfunction

• contaminated wound or umbilical stump in neonates
• incubation period: 3-14d = time to first symptom
• rigidity (persists > 2 weeks) — trismus, dysphagia, increased tone in trunk muscles – greater on side of injury initially
• spasms (reduce after 2 weeks) — spontaneous or provoked by physical or emotional stimuli, laryngospasm, risus sardonicus, opisthotonos (severe spasm in which the back arches and the head bends back and heels flex toward the back)

• autonomic disturbance (onset after spasms, lasts 1-2 weeks) — tachycardia and hypertension may alternate with bradycardia and hypotension, dysrhythmia, cardiac arrest — salivation, bronchial secretions — gastric stasis, ileus, diarrhoea
• respiratory compromise — chest wall rigidity — laryngospasm — aspiration — retained secretions

Td Prophylaxis:

• Past vaccination unknown or <3 total
  • Clean wound → Td
  • Dirty wound → Td & TIG
• Past vaccination 3 or more total
  • Clean wound → Td Q10yrs
  • Dirty wound → Td Q5yrs

Management:

A – intubate because management requires large doses of sedatives to control muscle spasm and to overcome laryngospasm B – at risk of aspiration and have copious bronchial secretions requiring frequent suctioning, often ventilated for 2-3 weeks until spasms subside C – autonomic dysfunction requires monitoring in a critical care environment D – benzodiazepines in large doses (up to 100mg/h diazepam)

Specific Therapy:

• metronidazole (first choice); penicillin is used throughout most of the world but is a GABA antagonist
• anti-tetanus immunoglobulin: 100-300IU/kg of human Ig IM
• benzodiazepines; adjuncts include barbiturates, propofol, chlorpromazine
• Mg to 2-4mmol/L as useful in spasm treatment and limits autonomic instability
• consider dantrolene (unproven)
• clean and debride wounds (source control)
• immunize (infection does not confer immunity) – Q10 yearly

Prognosis:

Mortality >50% if untreated (usually due to respiratory failure)

Sources: Life in the fastlane, WikiEM

Hip dislocations

Epidemiology:

-        rare, but high incidence of associated injuries

-        mechanism is usually young patients with high energy trauma

Simple vs. Complex:

o   simple

• pure dislocation without associated fracture

o   complex

• dislocation associated with fracture of acetabulum or proximal femur

-Anatomic classification:

o   posterior dislocation (90%):

• occur with axial load on femur, typically with hip flexed and adducted
• axial load through flexed knee (dashboard injury)
• hip and leg in slight flexion, adduction, and internal rotation
• examine knee for associated injury or instability

o   anterior dislocation:

• associated with femoral head impaction or chondral injury
• occurs with the hip in abduction and external rotation
• hip and leg in flexion, abduction, and external rotation

Imaging:

X-rays:

-        Can typically see posterior dislocation on AP pelvis

o   femoral head smaller than contralateral side

o   Shenton's line broken

o   Look at the femoral neck to rule out fracture prior to attempting closed reduction

o   AP pelvis after reduction to evaluate associated acetabular fractures

CT:

-        post reduction CT must be performed for all traumatic hip dislocations to look for:

o   femoral head fractures

o   loose bodies

o   acetabular fractures

Management:

1. Nonoperative
2. emergent closed reduction within 6 hours!
3.      indications:
4. acute anterior and posterior dislocations
5.      contraindications
6. ipsilateral displaced or non-displaced femoral neck fracture
7. Allis maneuver:

-        patient is placed in the supine position

-        knee is flexed to relax the hamstring

-        assistant stabilizes the pelvis

-        longitudinal traction is applied in line w/ axis of femur, and the hip is slightly flexed

-        gently adduct& internal rotates the femur to get reduction

https://www.youtube.com/watch?v=2dT1r_U7LQ8

2. Captain Morgan technique:

-        Position the patient: 90 degrees of hip and knee flexion

-        Step one foot up nto the gurney Captain-Morgan style (flamboyant cape optional).

-        Position your knee behind the patient’s knee.

-        Ideally your foot should be resting on a hard surface like a backboard to allow your foot to push off of it.

-        Place one hand (A) under the patient’s knee and the other (B) over the patient’s ankle.

-        Use Hand A to lift up on the patient’s femur.

-        Plantar-flex your ankle so that your propped knee can lift up on the patient’s femur

-        Very gently use Hand B to leverage-down on against the patient’s tibia/fibula.

https://www.youtube.com/watch?v=Uhkc7I4G7ng

2. Operative
   1. open reduction and/or removal of incarcerated fragments
   2.      irreducible dislocation
   3.      radiographic evidence of incarcerated fragment
   4.  delayed presentation 

1. ORIF
2. associated fractures of:
   1. acetabulum
   2. femoral head
   3. femoral neck

Sources: Ortho Bullets, ALiEM, Wheeless’ Textbook of Orthopaedics

TCA Toxicity

TCA is a sodium-channel blocker. The two main adverse effects of sodium-channel blocker poisoning include:

·       Seizures

·       Ventricular dysrhythmias (due to blockade of sodium channels in the CNS and myocardium)

 

In overdose, the tricyclics produce rapid onset (within 1-2 hours) of:

·       Sedation and coma

·       Seizures

·       Hypotension

·       Tachycardia

·       Broad complex dysrhythmias

·       Anticholinergic syndrome

 

·       Remember the 3 C’s: Coma, Convulsion, and Cardiotoxicity. So, get an EKG ASAP! 

 

What does TCA do exactly?

1.                    Blockade of myocardial fast sodium channels = QRS prolongation, and tall R wave in aVR

 

 

2.                    Inhibition of potassium channels= QTc prolongation, and direct myocardial depression.

3.                    Muscarinic (M1) receptor blockade= sinus tachycardia 

4.                    QRS > 100 ms is predictive of seizures

5.                    QRS > 160 ms is predictive of ventricular arrhythmias (e.g. VT)

 

Worsening TCA toxicity:

 

Management of Significant Tricyclic Overdose (> 10mg/kg) with Signs of Cardiotoxicity (ECG changes):

·       Don’t panic!

·       Intubate as soon as possible.

·       Hyperventilate to maintain a pH of 7.50 – 7.55.

·       IV, 02, monitor

·       Administer IV sodium bicarbonate 100 mEq (1-2 mEq / kg); repeat every few minutes until BP improves and QRS complexes begin to narrow.

·       Once the airway is secure, place a nasogastric tube and give 50g (1g/kg) of activated charcoal.

·       Treat seizures with IV benzodiazepines (e.g. diazepam 5-10mg).

·       Treat hypotension with a crystalloid bolus (10-20 mL/kg). If this is unsuccessful in restoring BP then consider starting vasopressors (e.g. norepinephrine infusion).

·       If arrhythmias occur, the first step is to give more sodium bicarbonate. Lidocaine (1.5mg/kg) IV is a third-line agent (after bicarbonate and hyperventilation) once pH is > 7.5.

·       Avoid Ia (procainamide) and Ic (flecainide) antiarrhythmics, beta-blockers and amiodarone as they may worsen hypotension and conduction abnormalities.

 

Sources: Life in the Fastlane, UpToDate