Post-operative complications Flashcards
Delirium
Acute confusional state, characterised by a disturbed consciousness and reduced cognitive function
Types of delirium
Hypoactive delirium – marked by lethargy and reduced motor activity
Hyperactive delirium – marked by agitation and increased motor activity
Mixed agitation – marked by fluctuations throughout a day
Delirium risk factors
Age > 65 years
Multiple co-morbidities
Underlying dementia
Renal impairment
Male gender
Sensory impairment (hearing/visual)
Delirium causes
Hypoxia
Infection
Drug-induced or drug withdrawal
Dehydration or pain
Constipation or urinary retention
Electrolyte abnormalities
Delirium investigations
Bloods – FBC, U&Es, Ca2+, TFTs, glucose
Blood cultures and/or wound swabs
Urinalysis and/or CXR
CT head
Delirium management
Any identified cause should be treated appropriately
Should be nursed in an appropriate environment & regular sleeping patterns promoted
Preventing worsening – oral fluid intake, provide analgesia & monitor bowels
Sedatives should be used sparingly – haloperidol is 1st line
Haemorrhage types
Primary – bleeding that occurs within the intra-operative period
Reactive – occurs within 24 hours of operation
Secondary – occurs 7-10 days post-operatively
Haemorrhage clinical features
Clinical features of haemorrhagic shock: tachycardia, dizziness, agitation, raised RR, decreased urine output
Examination – thorough exposure looking for bleeding, followed by systematic palpation of the surgical area looking for swelling, discolouration, disproportionate tenderness & any peritonism
Haemorrhage management
A to E approach – ensure adequate IV access and rapid fluid resus
Apply direct pressure to bleeding site if visible & urgent senior surgical review
Urgent blood transfusion, major haemorrhage protocol activated as necessary
May be appropriate to re-operate on patient for further haemostasis
Post-operative nausea and vomiting (PONV) risk factors
Patient factors – female, age, previous PONV, use of opioid analgesia, non-smoker
Surgical factors – intra-abdominal laparoscopic surgery, prolonged operative time, poor pain control post-operatively
Anaesthetic factors – opiate analgesia, inhalational agents, prolonged anaesthetic times, intraoperative dehydration, overuse of bag & mask ventilation
PONV pathophysiology
Two areas in the nervous system that play key role in the control of nausea and vomiting – vomiting centre & chemoreceptor trigger zone
Vomiting centre receives input from the chemoreceptor trigger zone, GI tract, vestibular system & higher cortical structures -> result in nausea
If stimuli are sufficient, acts on the diaphragm, stomach & abdominal musculature to initiate vomiting
PONV management
Prophylactic – anaesthetic measures, prophylactic antiemetic therapy, dexamethasone at induction
Conservative – adequate fluid hydration, adequate analgesia, consider NGT
Pharmaceutical
1) Patients with impaired gastric emptying/gastric stasis should be trailed on a prokinetic agent, such as metoclopramide (dopamine antagonist) or domperidone (dopamine antagonist), unless bowel obstruction suspected (hyoscine can be used instead)
2) Suspected metabolic/biochemical imbalance causing N&V can be trialled on metoclopramide
3) Opioid-induced N&V typically responds well to ondansetron or cyclizine
Consequences of poor pain control
Slower recovery – reluctant to mobilise, in turn resulting in a slower restoration of function and rehabilitation capacity
Patients in pain following abdominal surgery -> not breathe as deeply as they normally would and may not be able to cough to clear secretions resulting in inadequate ventilation and subsequent atelectasis & hospital-acquired pneumonia
NSAIDs side effects
I-GRAB
Interactions with other medications (eg. warfarin)
Gastric ulceration
Renal impairment
Asthma sensitivity
Bleeding risk
Opiate side effects
Constipation
Nausea
Sedation or confusion
Respiratory depression
Pruritus
Tolerance & dependence
Patient controlled analgesia
Involves the use of intravenous pumps that provide a bolus dose of an analgesic when the patient presses a button
Either started in theatre/in wards, when the use of strong oral opiates is inadequate
Can be titrated to give background infusions of analgesia if needed & the analgesic agent used can also vary
Post-operative pyrexia aetiology
Most common cause is infection:
Day 1-2: consider a respiratory source
Day 3-5: consider a respiratory/urinary tract source
Day 5-7: consider a surgical site infection or abscess/collection formation
Any day post-operatively: consider infected IV lines/central lines as a source
Other causes: iatrogenic, VTE, secondary to prosthetic implantation, PUO
Post-operative pyrexia investigations
Septic screen
Blood tests – FBC, CRP, U&Es, LFTs, clotting
Urine dipstick +/- urine MCS
Cultures – blood, urine, sputum & wound swab
Imaging – CXR, specific cross-sectional imaging
Post-operative pyrexia 5 Ws
Wind – chest infection
Water – UTI
Walk – DVT/PE
Wound – deep/superficial infection/collection
What have we done – drugs, lines, transfusion
DVT investigations
DVT wells’ score
Score less than/equal to 1 = requires a further D-dimer test to exclude
Score > 1 = DVT is clinically likely and a DVT diagnosis should be confirmed via either a ultrasound scan (more common) or contrast venography
DVT management
Direct oral anticoagulants (DOACs) – recommended as first line treatment for DVT
- Direct factor Xa inhibitors: apixaban, rivaroxaban, edoxaban
- Direct thrombin inhibitor: dabigatran
- Dabigatran and edoxaban require initial treatment with LMWH
Should be continued for 3 months in those with a provoked DVT
Proximal DVT and persistent risk factor/high risk of DVT recurrence – may require lifelong anticoagulation
PE investigation and management
PE wells’ score should be calculated
Score less than/equal to 4 = PE clinically unlikely, requires a further D-dimer test to exclude
Score greater than 4 = PE clinically likely & diagnosis should be confirmed with a CTPA scan (or V/Q scan in those with poor renal function/pregnancy/allergic to contrast)
Haemodynamically stable PEs – management is same as DVTs
Suspected PEs causing haemodynamic compromise – thrombolysis may be warranted
Thromboprophylaxis
All patients undergoing surgery should be offered mechanical prophylaxis unless otherwise contraindicated -> peripheral arterial disease, peripheral oedema or local skin conditions
Mechanical thromboprophylaxis – antiembolic stockings, intermittent pneumatic compression
Pharmacological – LMWH, unless poor renal function, then consider unfractionated heparin
Fat embolism syndrome
Rare but serious complication
Occurs with the introduction of fatty tissue into systemic circulation
Most commonly associated with long bone fractures, can also develops following routine orthopaedic procedures
Fat embolism syndrome risk factors
Young age
Long bone fractures
Closed fractures
Multiple fractures
Conservative management for long bone fractures
Fat embolism syndrome clinical features
Worsening SoB, confusion, drowsiness, development of petechial rash
Examination – tachypnoeic, tachycardia & hypoxic
Low-grade pyrexia
Gurd’s criteria used for diagnosis
Fat embolism syndrome investigations
Routine bloods – FBC, CRP, U&Es, LFTs and clotting screen
ABG
Blood film – may show presence of fat globules
CXR – diffuse bilateral pulmonary infiltrates
CTPA – ground-glass changes with a global distribution
Fat embolism syndrome management
Largely supportive, respiratory support is the mainstay of management
Prevention – limiting the dispersion of bone marrow into the blood stream, continuous pulse oximetry in patients undergoing IM nailing
Anastomotic leaks
A leak of luminal contents from a surgical join
Anastomotic leak risk factors
Patient factors – medication, smoking/alcohol excess, diabetes mellitus, obesity/malnutrition
Surgical factors – emergency surgery, longer intra-operative time, peritoneal contamination, oesophageal-gastric/rectal anastomosis
Anastomotic leak clinical features
Abdominal pain and fever
Usually present between 5-7 days post-operatively
Examination – pyrexial, tachycardic and/or with signs of peritonism
Anastomotic leak investigations
CT scan with contrast of abdomen and pelvis
Ensure early resuscitation and senior input
Urgent blood tests – FBC, CRP, U&Es, LFTs and clotting screen
VBG
Repeat group and save
Anastomotic leak management
Initial – NBM and start broad spectrum abx cover, IV fluid therapy and insert urinary catheter
Definitive – minor leaks usually settle with IV abx, larger ones commonly need to be drained percutaneously
Exploratory laparotomy is often required if patient is septic/multiple collections
Post-operative constipation aetiology
Physiology – low fibre diet, poor fluid intake, low physical activity
Iatrogenic – opioid analgesia, anticonvulsants, iron supplements or antihistamines
Pathological – hypercalcaemia, hypothyroidism, neuromuscular disease
Functional – painful defecation
Post-operative constipation clinical features
Lower abdominal pain, abdominal distension, N&V, decreased appetite
Examination – no clinical signs
DRE essential to assess the degree of faecal impaction
Post-operative constipation management
Conservative measures – adequate hydration, sufficient dietary fibre, treating the underlying cause & encouraging early mobilisation
Pharmacological:
- Osmotic laxatives: increased the amount of fluid in the bowel thereby softening stool – lactulose, Movicol
- Stimulant laxatives: stimulate the bowel to contract thus expelling faeces – senna, picosulphate
- Bulk forming laxatives: help stool to retain water thereby softening stool – ispaghula husk
- Rectal medications – glycerin suppository, phosphate enema
Post-operative ileus
Deceleration or arrest in intestinal motility following surgery
Functional bowel obstruction
Post-operative ileus risk factors
Patient factors – increased age, electrolyte derangement, neurological disorders, use of anti-cholinergic medication
Surgical factors – use of opioid medication, pelvic surgery, extensive intra-operative intestinal handling, peritoneal contamination, intestinal resection
Post-operative ileus clinical features
Failure to pass flatus or faeces
Sensation of bloating and distension
Nausea and vomiting
Abdominal distension and absent bowel sounds (mechanical obstruction = tinkling bowel sounds)
Post-operative ileus investigations
Initial routine bloods
CT scan abdomen and pelvis
Post-operative ileus management
NBM, ensuring adequate maintenance IV fluids
Daily bloods
Encourage mobilisation
Reduce opiate analgesia
Surgical site infection
Infection that occurs in the incision created by an invasive surgical procedure
Superficial – limited to skin and subcutaneous tissue
Deep – affecting the fascial and muscular layers
Cavity space infection – abdominal or joint cavity
Surgical site infection risk factors
Patient factors – increasing age, poor glucose control, obesity, smoking, renal failure, immunosuppression
Operation factors – preoperative shaving, length of operation, use of antimicrobial prophylaxis, appropriate skin preparation, appropriate gowning and sterile equipment
Surgical site infection clinical features
Typically appear 5 to 7 days post-procedure
Spreading erythema
Localised pain
Pus/discharge from the wound
Persistent pyrexia
Surgical site infection investigations
Wound swabs taken for culture at the wound site
Blood tests for infection markers should be taken, alongside blood cultures
Consider cross-section imaging to assess for deep collections
Surgical site infection management
Any sutures/clips present should be removed -> allowing for the drainage of any pus & opportunity for wound packing
Empirical antibiotics
Surgical site infection prevention
Pre-operative phase – prophylactic abx, do not remove hair routinely, patient advice (weight loss, smoking cessation, optimise nutrition, diabetic control)
Intraoperative phase – prepare the skin before the incision using an antiseptic preparation, change gloves/gown if contaminated, wound irrigation & use of antibiotic-impregnated sutures
Post-operative phase – monitor wounds closely, refer to tissue viability nurse for advice on appropriate dressings
AKI
> /= 50% rise in serum creatinine from baseline within last 7 days
Increase in serum creatinine by 26.5mmol/L within 48 hours
Urine output <0.5mls/kg/hour for more than 6 hours
Severity of AKI:
- Stage 1 – 1.5-1.9 times the baseline
- Stage 2 – 2-2.9 times the baseline
- Stage 3 = >3 times the baseline
Pre-renal AKI causes
Sepsis
Dehydration
Haemorrhage
Cardiac failure
Liver failure
Renal artery stenosis
Intra-renal AKI causes
Nephrotoxins – NSAIDs, ACEi, antibiotics (aminoglycosides), chemotherapy
Parenchymal disease – glomerulonephritides, acute tubulointerstitial nephritis, rhabdomyolysis, haemolytic uraemic syndrome or multiple myeloma
Post-renal AKI causes
Ureteric – retroperitoneal fibrosis, bilateral renal stones, tumours
Bladder – acute urinary retention, blocked catheter
Urethral – prostatic enlargement (BPH/malignancy), renal stones
Post-operative AKI investigations
Examine patient & fluid status
Bladder scan – evidence of retention, review drug chart
Urine dip
Initial bloods – U&Es, FBC, CRP, LFTs & Ca2+
Blood gas in severe cases
Imaging – USS of the kidneys, ureters & bladder is required in severe cases of AKI
Urine dipstick and differentiating causes of AKI
Can aid in differentiating between pre-renal and intrinsic causes of AKI
Urine specific gravity & osmolality values will be higher in pre-renal causes, urine Na excretion will be lower due to kidney actively conserving Na and water in pre-renal causes compared to intrinsic causes
Any glomerulonephritis will show high levels of blood and protein
AKI management
Fluid status – assess patient’s hydration status
- Pre-renal: give a fluid bolus & re-assess their fluid status after 10-15 minutes, monitoring the urine output after the bolus, give repeat fluid boluses until the patient is euvolaemic
Ongoing monitoring – start monitoring urine output, regular blood tests
Drug rationalisation
1) Drugs to be stopped: ACEi/ARBs, NSAIDs, aminoglycoside antibiotics, potassium-sparing diuretics
2) Drugs to be altered or reduced: metformin (risk of lactic acidosis), diuretics, LMWH
Post-operative urinary retention
Acute urinary retention – symptomatic inability to completely empty the bladder
Post-operative urinary retention clinical features
Little/no urine passed in the post-operative period
Sensation of needing to void without being able to micturate
Suprapubic mass that is dull to percussion
Assessed for any underlying causes – uncontrolled pain constipation, infection, anaesthetic agents (spinal/epidural)
Post-operative urinary retention risk factors
Age > 50 years
Male gender
Previous retention
Type of surgery – including pelvic/urological surgery
Anaesthetic type – spinal or epidural
Neurological/urological co-morbidities
Medication (eg. antimuscarinics, alpha agonists, opiates)
Post-operative urinary retention assessment
Most important investigations – ultrasonic bladder scan to identify the post-void residual urine volume
Check for any potential underlying reversible causes & that there is adequate pain control
Check patient has a stable renal function (worsening renal function may suggest a high-pressure retention that is impacting renal function)
Post-operative urinary retention management
Conservative management – majority of post-operative urinary retention will resolve spontaneously
In those that don’t resolve – any significant retention will require catheterisation, patients can have their catheter removed shortly after (TWOC)
For those who fail TWOC & re-enter retention, a new catheter should be inserted & patients for repeat TWOC in 1-2 weeks in the community
Make sure to re-assess any potential reversible causes why the patient may have failed their TWOC that can be addressed
Post-operative UTI organisms
E. coli
Klebsiella sp.
Enterobacteur sp.
Proteus sp.
Pseudomonas sp.
Staphylococcus sp.
Post-operative UTI risk factors
Age > 60 years
Female
Significant co-morbidities
Catheterisation or recent instrumentation
Pregnancy
Urinary retention or renal stones
Post-operative UTI clinical features
Urinary frequency, urgency & dysuria
Examination – mild suprapubic pain & be pyrexial
Should be considered in any patient who presents: with delirium, sepsis, in acute urinary retention
Assess for features of pyelonephritis – loin pain, renal angle tenderness or pyrexia
Sterile pyuria
Presence of an elevated WCC in the urine, however no organisms are identified using standard culture techniques
Causes of sterile pyuria – inadequately-treated UTI, STI or renal stones
Post-operative UTI investigations
Urine dipstick should be performed initially (despite high risk of contamination seen in elderly population)
Urine dipstick is positive or clinical features in keeping with UTI = urine should be sent off for MC&S
Routine blood tests may be considered, blood cultures and VBG
Bladder scan may be required if patient has potentially entered retention
If pyelonephritis is suspected/in cases of recurrent UTIs – a renal US or further definitive imaging may be required to check for obstructive causes
Post-operative UTI management
Ensure patient is well hydrated and maintains a satisfactory urine output
Definitive management is via antibiotic therapy, classically trimethoprim, nitrofurantoin or co-amoxiclav
Adapt abx choice accordingly following MC&S results if poor response, any catheterised patients with a UTI should have their catheter changed prior to starting any antibiotics
Post-operative haemorrhage neck surgery
Post-operative thyroidectomy or parathyroidectomy haemorrhage – primary sign is likely to be airway obstruction
- Pretracheal fascia of the neck will only distend so far, when bleeding occurs into this space, compression on the venous return results in venous congestion, with subsequent laryngeal oedema leading to eventual asphyxiation
Any evidence of respiratory distress/airway compromise in these patients requires an emergency protocol for airway rescue -> removing both the skin clips and deep layer sutures & suction of the haematoma beneath (all done at bedside)
Post-operative haemorrhage inferior epigastric artery injury
Inferior epigastric arises from the external iliac artery & runs up the abdominal wall below the rectus muscle -> vulnerable to injury from laparoscopic ports
Due to the gas insufflation, this may not be noticed at the time of surgery
Particularly after laparoscopic surgery or surgery with a Pfannenstiel incision
Post-operative haemorrhage retroperitoneal bleeding post-angiography
Puncture site is often the external iliac artery, above the inguinal ligament -> any bleeding from this artery can track into the retroperitoneum
Likely not be a large haematoma around the skin puncture site, because the actual arterial puncture site is hidden by the inguinal ligament
Patients will often bleed profusely because tamponading the injury is difficult
For any suspected occult retroperitoneal haemorrhage, apply pressure to the puncture site, resus, ensure blood products are made immediately available & call for senior support
Cross-sectional imaging to confirm the diagnosis is often required
Keloid
Abnormal proliferation of scar tissue which forms at the site of injury, rises above the skin level, projects beyond original wound margins
Affects both men and women equally, with the highest incidence occurring between the ages of 20 and 30
Keloid pathophysiology
Normal wound healing, there is a balance between new tissue biosynthesis and tissue degradation – achieved through the processes of apoptosis and remodelling of the ECM
During keloid formation, there is prolonged inflammatory phase -> contributes to excess fibroblast activity and increased deposition of ECM, resulting in the tissue projecting beyond the original wound margin
Keloid risk factors
Ethnicity – most common in black African or Caribbean and Asian populations
Age – the highest incidence occurring between 20-30 years
Causes – burns carry the highest risk
Anatomical site – most commonly occur in scars on the ear lobe, shoulders and sternal notch
Previous keloid formation
Keloid clinical features
Characteristic visual appearance – keloid scars are raised above the skin around them and can take on the appearance of a dome shape, extending beyond the original wound margin, shiny and hairless
Do not normally cause may other symptoms – small proportion of patients experience of pain, itching or burning in the scar tissue
Keloid management
Surgical excision is rarely performed – thought to stimulate collagen synthesis -> results in the regrowth of a larger keloid
Non-surgical management
1) Intralesional steroids – acting as anti-inflammatory agent that inhibits the fibroblast glucocorticoid receptors, this in turn downregulates the proliferation of fibroblasts and inhibits collagen synthesis
2) Silicone gel – either as a topical gel or as an elastic sheet
3) Radiation therapy – reduces the recurrence of keloids, especially as an adjunct therapy (runs the theoretical risk of inducing malignancy which has limited its potential use)
Wound dehiscence
Wound fails to heal, often re-opening a few days after surgery (most common in abdominal surgery)
Superficial dehiscence – skin wound alone fails, with the rectus sheath remaining intact
- Occurs secondary to local infection, poorly controlled diabetes or poor nutritional status
Full thickness dehiscence – rectus sheath fails to heal and bursts, with protrusion of abdominal content
- May occur secondarily to raised intra-abdominal pressure, poor surgical technique or if patient is critically unwell
Wound dehiscence risk factors
Patient factors – increasing age, male gender, co-morbidities (diabetes), steroids, smoking, obesity/malnutrition
Intra-operative factors – emergency surgery, abdominal surgery, length of operation, wound infection, poor surgical technique
Post-operative factors – prolonged ventilation, post-operative blood transfusion, poor tissue perfusion, excessive patient coughing, radiotherapy
Wound dehiscence clinical features
Visible opening of the wound, healing poorly following the operation
Typically happens around 5-7 days post-operatively
Classic signs of full thickness dehiscence – new building of the wound and seepage of pink serous or blood-stained fluid from the wound
Superficial dehiscence management
Wash wound out with saline and then simple wound care – packing the wound with absorbent ribbon gauze
Patient should be advised the wound will now be required to heal by secondary intention & can take several weeks
More extensive wounds may be treated with a vacuum-assisted closure device to speed healing
Full thickness dehiscence management
Provide suitable analgesia and start broad spectrum IV abx as a priority
Cover the wound in saline-soaked gauze and arrange urgent return to theatre for re-closure of the wound
For majority of the patients, closure is usually done in theatres with large interrupted sutures, avoiding excessive tension
If there is gross abdominal sepsis, necrotising fasciitis of abdominal wall -> can be managed as an open abdomen (using a vacuum dressing) or using a bridging mesh
Wound dehiscence prevention
Optimisation of co-morbidities and treating any surgical site infections is key
Avoiding heavy lifting and encouraging adequate post-operative nutrition will reduce the risk further
