laryngospasm

LARYNGOSPASM
Laryngospasm is the reflex adduction of the vocal cords in response to irritation of the airway (e.g. secretions, blood, vomit and laryngoscopy) or in response to noxious stimuli during light anaesthesia.

RISK factors:
Patient factors-
-young patients
-URTI
-hyperreactive airways
Surgical factors-
-airway surgery, supraglottic airway devices

Presents with a crowing inspiratory noise in the case of partial obstruction. There may not be any noise in the case of complete obstruction
Paradoxical breathing, tachypnea, arrhythmias. Hypoxaemia, hypercarbia. REDUCED MOVEMENT OF RESERVOIR BAG
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This is an urgent situation which may lead to desaturation and severe morbidity
I would examine the patient immediately and check the SpO2 and attempt manual ventilation.
If there is normal SpO2 or decreasing SpO2:
-if there is difficulty ventilating the patient due to severe spasm or desaturation, I would
-ask the surgeon to halt the stimulus and increase the FiO2 to 1.0.
-provide CPAP
-deepen the anaesthesia using and IV agent such as propofol 20mg. Alternatively I could increase the concentration of inspired inhalational anaesthetics but given the degree of laryngospasm it may not be sufficient.
-If I am unable to ventilate or improve the saturations due to severe laryngospasm, I will give a small dose of IV suxamethonium 0.1-0.5mg/kg. If severe a full dose may be given and the trachea intubated.

-if normal SpO2:
-deepen anaesthesia
-CPAP
-analgesia

-other manouveres: forcible jaw thrust, pressure on the mandible at Larson’s point (anterior to the mastoid process)
-if no IV: !M sux or into the tongue 3mg/kg

LA toxicity

(Sep-2003 Q7) At the end of an open cholecystectomy, intercostal nerve blocks with a total of 20ml bupivacaine 0.5% are placed at two levels while the patient is still under general endotracheal anaesthesia. The patient develops ventricular fibrillation within 3 minutes. Describe your management of this situation.

The patient has received 20x5mg =100mg of bupivacaine and the weight of the patient is not known here but given the short duration prior to cardiac arrest, the most likely differential in this situation is cardiovascular collapse from LA toxicity. Other less likely differentials would be a acute coronary event due to underlying ischaemic heart disease or arrhythmias.
The immediate management of this patient will include resuscitation according to BCLS protocols while maintaining the airway and breathing by leaving the patient intubated, 100% O2 and commencing CPR and defibrillation. IV adrenaline boluses 1mg of 100mcg/ml dilution and magnesium may be given. ?phenytoin.

Lipofundin as been shown to be effective in ???? it is available as given via a large bore IV line as a rapid bolus of 100ml followed by 400ml

The surgical team and family has to be informed and the patient admitted to SICU after successful resuscitatoin. ? maintainence lipofundin?Incident reporting and post event counselling.

Fat embolism syndrome

(May-2008 Q4) Describe the clinical features and treatment of Fat Embolism Syndrome.

Clinical features:
1) hemodynamic changes: tachycardia, hypotension, desaturation
2) ECG changes: right heart strain , RV failure
3) End tidal CO2 : marked reduction due to reduced preload and cardiac output
4) Clinical: confusion, dyspnea, petechiae

Treatment:
1) initial stabilisation, 100%O2, diuretics ventilatory support and endotracheal intubation if necessary
2) CVP, aspiration of embolus ??
3) Monitoring for complications eg ARDS, DIVC
4) Arterial blood gas and 12 lead ECG
5) early fracture fixation
6) controversial: heparinisation, corticosteroids


Marks for situations where FES is likely to occur

Diagnostic criteria (combined from various sources)
Diagnostic criteria were first devised by Gurd and have been modified several times since.8,9
Major criteria
• Respiratory insufficiency
• Cerebral involvement
• Petechial rash
Minor criteria
• Tachycardia
• Pyrexia (usually >39°C)
• Confusion
• Sustained pO2 <8 kPa • Sustained respiratory rate >35/minute, in spite of sedation
• Retinal changes - cotton wool exudates and small haemorrhages, occasionally fat globules seen in retinal vessels
• Jaundice
• Renal signs
• Thrombocytopenia
• Anaemia
• High ESR
• Fat macroglobulinemia
• Diffuse alveolar infiltrates 'snow storm appearance' on chest X-ray


Causes
• Fractures - closed fractures produce more emboli than open fractures. Long bones, pelvis and ribs cause more emboli. Sternum and clavicle furnish less. Multiple fractures produce more emboli
• Orthopaedic procedures - most commonly intramedullary nailing of the long bones, hip or knee replacements4
• Massive soft tissue injury
• Severe burns
• Bone marrow biopsy
• Nontraumatic settings occasionally lead to fat embolism. These include conditions associated with:
o Liposuction5
o Fatty liver
o Prolonged corticosteroid therapy
o Acute pancreatitis
o Osteomyelitis
o Conditions causing bone infarcts, especially sickle cell disease



Presentation
There is usually a latent period of 24 to 72 hours between injury and onset. The onset is then sudden, with:
• Breathlessness ± vague pains in the chest. Depending on severity this can progress to respiratory failure with tachypnoea, increasing breathlessness and hypoxia.
• Fever - often in excess of 38.3°C with a disproportionately high pulse rate.
• Petechial rash -commonly over the upper anterior part of the trunk, arm and neck, buccal mucosa and conjunctivae. The rash may be transient, disappearing after 24 hours.
• Central nervous system symptoms, varying from a mild headache to significant cerebral dysfunction (restlessness, disorientation, confusion, seizures, stupor or coma).
• Renal - oliguria, haematuria, anuria.
• Drowsiness with oliguria is almost pathognomonic.


Predictors of fat embolism
- long bone fractures (excluding NOF)
- multiple fractures

myasthenia gravis

tutorial today by Dr Hari - question was apparently asked in oct 2009

you are an anaesthetist in a rural hospital and the obstetrician calls you regarding an emergency CS for NRFS. She also has a past history of myasthenia gravis

1) how do you go about determining the degree of NRFS

-use of CTG - presence of late or variable decelerations, defined as decrease in HR of more than 15 beats lasting at least 30 s

-use of scalp pH (normal pH of neonate 7.25-7.35), so fetal distress is when scalp pH <7.25

2) how do you go about assessing this patient for op

don't just focus on the obstetric history- placenta praevia, antenatal history, GDM, lie etc, gestation

-history

-clinical exam

-go through relevant investigations

-old notes

history: extent of disease, control, recent exacerbations esp due to pregnancy

medications: pyridostigmine dose, steroids, immunosuppressants, plasmapheresis

autonomic instability

pre op PFT

issues of post op ventilation:

management: pre op aspiration prophylaxis, neonatologist, wedge , warm OT for baby

standard monitoring, airway trolley and difficult airway adjuncts, experienced surgeon, colleague to help with anaesthesia, AU

working IV plug

maintain with 02:n2o:inhalational, use bis to reduce amount of inhalational (potentiate nm weakness), nerve stimulator

pharmaco: duration of action of sux : unpredictable, may require higher dose eg 2mgkg

high dose may cause type 2 blockade, onset delayed

if on regular plasmapheresis, enzyme to metabolise sux may be reduced

increased sensitivity to relaxant

if not given usual meds preop: controversial- give IV neostigmne 1:30mg pyrido or NG pyrido?

non depolarising: give 1/10 of usual dose, titrate to nerve stimulator

• Ensure that the patient is reminded prior to induction of the possibility of a prolonged intubation*

Extubation: performed on awake patients and hopefully close to his/her baseline status. Reinstitute anticholinesterase medication, either by IV infusion or by reimplementation of the patient's oral regimen.

Leventhal criteria: Predictive scoring system for the need for postoperative ventilation

1) duration of disease for 6 years or longer

2) chronic comorbid pulmonary disease

3) pyridostigmine dose >750 mg/d

4) VC <2.9L

5) Other indicators include preoperative use of steroids, and previous episode of respiratory failure.

These predictors have not been widely validated. (1)

Drugs to avoid: Calcium Channel blockers, Magnesium, Aminoglycoside antibiotics as all of these may contribute to muscle weakness

Post-Op Bed: Patients should be monitored in either a ICU or step-down unit but NOT to a conventional surgical ward.

3) MG vs eaton lambert,

tensilon to differentiate

4) baby not breathing , mother not stable

priority is to stabilise mother

baby: SpO2 88% Hr 50, chin lift and BVM (? pressure gauge), towel under shoulders. intubate , start CPR

CVS collapse most likely due to hypoxia

call code blue, adrenaline 10mcg/kg

stop CPR when HR >60

ETT adrenaline 100mcg/kg (other routes IM, umbilical)

resus guidelines :ARC

5) PPH: anaes plan

-defined as? >500ml/24h

-fluid resus

-post partum : assum gastric physiology and aspiration risk still present up to 48h

-issues of recent GA, physiology changes, MG

AIMS anaesthesia analysis

http://www.apsf.com.au/crisis_management/crisisframe1_frame1.htm

THE BASIC ALGORITHM
commit to memory
C Circulation Capnograph Colour (Saturation)
O Oxygen Supply Oxygen Analyser
V Ventilation (Ventilated Pts) Vaporisers
E Endotracheal Tube Eliminate Machine
R Review Monitors Review Equipment

A Airway (if Face mask or LMA)B BreathingC Circulation (in more detail)D Drugs

A Awareness Air embolism Air in pleura Anaphylaxis

SWIFT CHECK of Patient, Surgeon and Surrounds

Change order for spontaneous breathing to:AB COVER CD A SWIFT_CHECK