Gen Surg Flashcards
GEN SURG – CO2 embolism
[21B04] Describe the clinical presentation of venous carbon dioxide embolism during laparoscopic surgery and outline your management.
differentiate b/w VAE!
CO2 microembolism occurs
Presentation
1. Gas exchange abn
- low O2, CO2, pH
2. Inc RV AL
3. Dec LV filling
- Dec CO/ LV failure / cardiac arrest
Mx
- Notify surgeons
- Desuffl
- Left lat decub
- 100% O2
- CVC
- HBOT
GENERAL – ECG after LBO Laparotomy (inferior ischaemia)
[21A05] This is the standard 12-lead electrocardiogram (ECG) of a 56-year-old man in the post-anaesthesia care unit (PACU) two hours after an emergency laparotomy for bowel obstruction. He is complaining of SOB, abdominal pain and has a blood pressure of 160/110mmHg.
He has a history of hypertension controlled with atenolol and hydrochlorothiazide. The preoperative ECG is missing. The anaesthetic assessment only notes that it showed sinus rhythm.
Considering all the clinical information:
a) Interpret this ECG
b) Outline the appropriate management of this patient in PACU.
Interpret:
- Mx of ischaemia
MOAN - HTN mx
- Imm post op
- Thrombolysis less appropriate
GENERAL – Autonomic dysreflexia
[19A08] A patient with previous spinal cord injury presents for ureteric stenting.
a) Discuss the pathophysiology of autonomic dysreflexia. (50%)
b) Describe the intraoperative manifestations and subsequent management of autonomic dysreflexia. (50%)
Pathophysiology
- Autonomic dysreflexia = medical emergency characterised by uncontrolled SNS response due to a precipitant. o Occurs in up to 90% of patients with SCI at T6 or above
o Occurs weeks ® 1 year after injury
- Triggers
o Bladder = distension, irritation, UTI
o Bowel = distension, constipation, haemorrhoids
o Other = skin infection/abrasion, injury, tight/restrictive clothing
- Mechanism:
o Stimulus below level of lesion
o Afferent impulses transmitted to spinal cord ® unable to pass level of injury ® reflex activated causing SNS activity
o Vasoconstriction of splanchnic + peripheral circulation causing systemic HTN
o Baroreceptors detect BP ® activate descending inhibitory PNS activity, but unable to pass below level of lesion
o Unopposed SNS activity below level of lesion ® severe HTN + reflex bradycardia
o Level of SCI determines the autonomic control of the splanchnic circulation
o Greater splanchnic nerve arises from T5-9 ® therefore lesions above T6 constrict the splanchnic bed causing profound HTN, while
lesions below allow more PNS inhibitory control, preventing HTN
Clinical features
- Depend on level and completeness of lesion:
o Sudden HTN ( SBP 20-40mmHg ® may result in ICH, seizures, ACS< APO)
o Bradycardia (HR < 60)
o Headache
o Above level of lesion = PNS (flushing, sweating, pupillary constriction, nasal congestion) o Below level of lesion = SNS (pallor, piloerection)
Management
- Declare medical emergency, communicate with surgeons
- Sit pt up where possible, remove tight clothing
- Exclude common triggers (bladder distension, constipation) - Treat HTN:
o SL GTN 300-600mic
o IV hydralazine 10-20mg
o IV GTN, MGSO4, phentolamine, clonidine, papaverine)
(54.8%) In the first part of the question the candidate was required to demonstrate a clear understanding of the pathophysiology with emphasis on factors such as the time since spinal cord injury and spinal cord level of injury. In the second part of the question application of this knowledge to the intra-operative situation was required. Examiners were looking for a clear description of the autonomic manifestations and the emergent management of the cardiovascular problems.
