Care of surgical patients Flashcards
Causes of pyrexia post-op?
Infection: 1-2d resp, 3-5d UTI, 5-7d surgical site/abscess, any day consider infected IV/central line
Iatrogenic: malignant hyper-pyrexia, transfusion reactions
VTE: may cause low fever
PUO: recurrent fever >38 for >3w without obvious cause despite >1w inpatient investigation
Causes of tachycardia post op?
Pain, anxiety, infection, thyrotoxicosis, hypovolaemic shock, recent onset AF/flutter, anastomotic leak
Cause of sudden collapse/deterioration post op?
CVS-MI, PE, stroke
Resp-failure of reversal of anaesthesia, hypoxia
Surgical-hypovolaemia, bowel obstruction, sepsis
Metabolic-electrolytes, hypoglycaemia, adrenal insufficiency
Anaphylaxis
Cause of N&V post op?
Drugs: opiates, erythromycin, metronidazole
Immediately post-op: vestibular, oropharyngeal stimulation from NGT, hypotension, pain, anxiety
Bowel obstruction: mechanical, dynamic bowel or faecal impaction
Systemic disorders like uraemia, RICP
Haematemesis
Cause of bowel dysfunction post op?
Diarrhoea: common transient post-ado surgery, C diff
Constipation: common due to restricted fluids + fibre, reluctancy using bed pan, slow recovery of peristalsis, opiates, lack of mobility. Hydration, fibre, mobilise, osmotic laxatives e.g. lactulose, stimulants e.g. senna, bulk-forming e.g. ispaghula husk, glycerine suppositories, phosphate enemas
Cause of poor urine output post op? (<0.5ml/kg/hour)
Pre-existing bladder outlet obstruction, embarrassment, overfilling bladder during operation, neurological disturbance from GA/spinal, pain from abdo wound, constipation, hypovolaemia, reduced CO, AKI
Post-op delirium - causes + workup
Acute confusional state, disturbed consciousness + reduced cognitive function. Short term + fluctuating, commonly get hallucinations/delusions, hypoactive > hyperactive
Causes: Hypoxia, infection, drugs (BZDs, diuretics, opioids, steroids), dehydration, pain, constipation, urinary retention, endocrine issues
Workup: collateral hx, AMT, CAM, review obs + drugs + signs of infection, neuro examination to r/o stroke/SDH, bloods (FBC, U+E, Ca, TFT, glucose, poss haematinics/blood culture/wound swabs), urinalysis, CXR, CT head if indicated
Cause of respiratory problems post op?
ARDS: severe hypoxaemia from inflammatory damage to alveoli - pulmonary oedema - damaged T2 pneumocytes so less surfactants. Direct (pneumonia, smoke, aspiration, fat embolism) + indirect (sepsis, pancreatitis) causes. High mortality + progression to pulmonary fibrosis. Causes sob, cyanosis, hypoxia, tachycardia/pnoea, inspiratory crackles, CXR shows diffuse b/l infiltrates (like pulmonary oedema). M is supportive (ventilation), treat cause, need ITU
Atelectasis: partial collapse of small airways, occurs in most post-op to some extent within 24h. Less expansion - pulmonary secretions accumulate - hypoxaemia, reduced compliance, increased infection. RF include smoking, GA, longer operations, underlying lung/NM disease, poor pain control. M: deep breathing, physio, analgesia
Pneumonia: HAP >48h post-admission. Due to reduced ventilation or change in commensals e.g. E coli/S aureus etc. P/w pneumonia CF inc impaired cognition, cannot use CURB65
Aspiration pneumonia: of gastric contents – chemical pneumonitis and poss infection depending on if bacteria get in, usually RML/RLL. RF: reduced GCS, NGT, prolonged vomiting, neuro problems, and post-abdo surgery. M: SALT, supportive, Abx if infection
Post-op bowel complications
Anastomotic leaks: leak of luminal contents from surgical join between two hollow viscera, causes signs of peritonism + sepsis + prolonged ileus, check wound drain for faeculent/purulent/bilious matter. RF include emergency/big ops, peritoneal contamination, rectal anastomosis, meds, smoking, alcohol, DM, obesity. M: NBM, brand spec Abx, catheterise, minor leaks bowel rest + percutaneous drainage, major need laparotomy
Bowel adhesions: fibrous bands that cause SBO, most conservative (tube decompression, NBM, fluids, analgesia), surgery if >48h or perforation or ischaemia
Incisional herniae: as have made a weakness, common, can strangulate etc. RF: emergency surgery, wound type, raised BMI, midline incisions, wound infection, pre-op chemo, intra-op blood transfusion, older pt, pregnant pt
Constipation: most often from paralytic ileus but can be cos of low fluid/low fibre, drugs e.g. opioids, functional (e.g. painful defecation), pathological (e.g. bowel obstruction, hypercalcaemia, hypothyroidism). Risk increased with intra-op bowel handling, low mobility. DRE may show faecal impaction. M: hydration, fibre, mobilising, osmotic laxatives (increase fluid to soften it so lactulose/movicol), stimulant laxatives (cause contraction so senna, picosulfate), bulk-forming laxatives (retain water like ispaghula husk), rectal stimulants (phosphate enema, glycerine suppository). Stimulant used for ileus/opioid/soft stool, stool softener + suppositories for hard stool
Post-op ileus: intestinal motility stops causing functional obstruction, common and usually goes away (tho can be because of anastomotic leaks). RF include pt age/electrolytes/meds, surgical opioids/bowel handling/intestinal resections), causes absolute constipation, distention, N&V/high NG output, absent BS (whereas mechanical obstruction=tinkling bowel sounds). If not improving do CT. M-daily bloods, mobilise, reduce opiates.
Electrolyte abnormalities + ECG changes
Hyperkalaemia - causes include AKI, K+ sparing diuretics, ACEi/ARB, repeated blood transfusions, excess K+. ECG may show tall T waves, long PR, flattened P, prolonged QRS, widened QRS, axial deviation + BBBs, sine wave pattern, VF, asystole. High levels may cause paraesthesia, muscle weakness, N+V, palps. M: stabilise myocardium (IV calcium chloride/gluconate), reduce serum K+ (VRII + dextrose), salbutamol nebs, reverse cause
Hypokalaemia: causes include TD/LD/steroids/excess insulin/salbuamol/D+V/hyperaldosteronism/burns/inadequate replacement in fluids/malnutrition/Cushing’s/low magnesium.. ECG may show long PR, T flat/inverted, prominent U wave, ST depression, VT/VF. Most asymptomatic but may cause muscle weakness, paraesthesia, constipation, hypotonia, hyporeflexia, cramps, tetany
Hypernatraemia: quite rare tbh, no ECG, sx when v high levels, may be hypovolaemic (diuretics/dehydration/acute tubular necrosis/HHS), euvolaemic from diabetes insipidus, or hypervolaemic from excess hypertonic saline/steroid excess. Can cause weakness, lethargy, irritable, confusion, ataxia, seizures, tremor, coma. M=replace fluid deficit, lower sodium by 10mmol/day (to reduce risk of cerebral oedema).
Hyponatraema: v common, no ECG changes. Hypovolaemic due to D+V or diuretics, euvolaemic due to fluid overload or SIADH or hypervolaemic due to HF/cirrhosis/acute tubular necrosis. Usually no sx but severe causes neuro signs as low plasma osmolality means fluid moves to ICF, in brain this causes RICP. Do not correct too rapidly as can cause central pontine myelinolysis (rapid change in ECG osmolarity damages myelin sheaths - balance issues, confusion, pseudobulbar palsy, quadriplegia). M: fluid balance, IV fluids with Hartmann’s/normal saline
Hypoglycaemia: due to iatrogenic, gastric dumping syndrome, decompensated liver disease, adrenal insufficiency. Causes sweating, tingling extremities/lips, tremor, dizziness, slurred speech, pallor, confusion, high HR/RR, focal neurology, reduced GCS. May not have signs with BB. M: if conscious give oral glucose rapid acting + complex carbs, if not IV glucose or IM glucagon if no access
Skin complications
Keloid scars -tissue projects beyond wound margins without regression, common after burns, recurrence common so don’t usually excise, can try intralesional steroids + silicone gel. (Ddx hypertrophic scar which is within confines of wound margin).
Surgical site infections - usually 3-7d after op, tho prosthetic infections up to several months. Most superficial. RF: age extremes, malnutrition, DM, CKD, smoking, other infection, immune suppressed, long hospital stay, operation length, foreign material, drains, poor closure, post-op hypothermia/haematoma/lymphatic leak. Remove sutures/clips to allow drainage, drain off pus, ABX, monitor for sepsis. Prevent by not routinely removing hair (only immediately before incision), preparing skin intra-op, ABX
Wound dehiscence - failure of wound to close properly. Simple (skin wound, often cos of infection/DM) vs burst (protrusion of abdo contents, often technique failure/raised abdo pressure). Commonest cause is infection, often need return to theatre for debridement + Abx. avoid heavy lifting, improve nutrition.
Abscess - mass of necrotic tissue, needs drainage + Abx
What is gastric dumping syndrome?
Post-gastrectomy at risk
Early after eating intraluminal fluid shift + intestine dilatation causes N, V, D
1-3h after eating surge in insulin following ‘dumping’ of food – hypoglycaemia
Manage by frequent small meals and E + D separately to avoid heavy loads
What general management would you apply pre-op?
Reassurance
Advice - stop eating 6h before, stop clear fluids 2h before
Prescriptions - various changes may be needed
Referral - consider if they will need HDU/ITU
Investigations
Observations
Patient understanding + follow up
What changes to medication may be needed pre-op?
Stop: clopidogrel (7d before [aspirin etc usually fine to continue]), hypoglycaemics (24h before), metformin on day of, COCP/HRT (4w before due to DVT), warfarin (5d before, INR needs to be <1.5)
Alter: SC insulin (sliding scale infusion), long term steroids (must be continued and probably increased due to the stress)
Start: LMWH (most except neck + endocrine), TED stockings (all except vascular + severe skin issues), AB prophylaxis (ortho, vascular, GI), bowel preparations
What bowel preparations may be needed for colorectal surgery?
Phosphate enema morning of surgery - left heme-colectomy, sigmoid colectomy or ado-perineal resection
Picolax the day before-anterior resection
Decreased in both serum + urine osmolality?
Overhydration, hyponatraemia, adrenocortical insufficiency
Decreased serum osmolality, increased urine osmolality?
SIADH
Normal/increased serum osmolality, decreased urine osmolality?
Diabetes insipidus
Normal/increased serum osmolality, increased urine osmolality?
Dehydration, renal issues, HF, Addison’s, hypercalcaemia, DM, hypernatraemia, alcohol
Outline the body fluid compartments in an average 70kg man
42L TBW
ICF 28L
ECF 14L – 3L intravascular, 11L extravascular (split to 10.5L interstitial + 0.5L transcellular)
What is the normal fluid output + input from?
Input - 60% from enteric route, rest food + metabolism
Output - urine and insensible losses (respiration, sweat and faeces - these rise during illness)
What are the clinical features of fluid overload?
Raised JVP, peripheral/sacral/pulmonary oedema
Orthopnoea, PND
What are the clinical features of fluid depletion?
Dry mucus membranes, reduced skin turgor, reduced UO (<0.5ml/kg/hr), orthostatic hypotension; more severe-increased CRT, hypotension, tachycardia, cold peripheries, tachypnoea, NEWS of 5 or more, dry axillae
How can you assess fluid status?
History
Examination
Fluid input-output chart + daily weights
U&E - dehydration, renal issues, hypovolaemia signs (high Na+, Hb, haematocrit), plasma osmolality (2 [Na + K] + urea + glucose), urea:creatinine ratio (raised in hypovolaemia as more urea reabsorbed)
Hypovolaemia + dehydration often occur together but what is the difference?
Hypovolaemia - loss of sodium + water, patient haemodynamically unstable, needs rapid fluid resus
Dehydration - loss of water but not sodium, can lead to hypovolaemia, patient hypernatraemic, needs oral rehydration/slow IV fluids
Why does bowel obstruction cause dehydration?
Fluids that are secreted accumulate but aren’t reabsorbed - isotonic contraction of ECF - dehydration + raised haematocrit
When vomiting lose ECF into gut lumen (also leads to metabolic alkalosis with low blood volume, Cl- and K+)
From where may excess fluid losses occur?
Vomiting/NGT - hypocholaraemic hypokalaemic metabolic alkalosis Biliary drainage Diarrhoea/colostomy High or lower volume ileal losses Pure water loss e.g. fever, dehydration, hyperventilation (potential for hypernatraemia) Pancreatic drain Jejunal loss Inappropriate urinary loss Ongoing blood loss
What are the daily fluid + electrolyte requirements NICE recommend?
Water 25-30 ml/kg/d
Na+, K+, Cl- 1mmol/kg/d
Glucose 50-100g/day
Why are crystalloids preferred over colloids?
Colloids: no role in maintenance, risk of anaphylaxis, coagulopathy and higher cost
Crystalloids lower risk and distribute throughout ECF as electrolytes go through membrane (whereas colloids larger proteins mean more likely to stay IV but this is theoretical)
Why to 0.9% NaCl + Hartmann’s distribute in the whole ECF?
Their [Na+] is similar to that of the ECF so only about 1/4 stays in the IV part of this. So e.g. for 100ml blood loss need 400ml 0.9% NaCl
What happens if you give too much NaCl?
Hypernatraemic, hypercholeraemic metabolic acidosis
How does 5% dextrose distribute?
Isotonic in the bag but the sugar is quickly metabolised so it becomes hypotonic so its the same as giving pure water – distributes throughout all compartments, only about 1/12 is IV so bad for resuscitation but good for dehydration/hypernatraemia replacement
How to prescribe maintenance fluids?
When patient can’t meet needs enterally but don’t have complex fluid/electrolyte issues – aim to match normal daily requirements as much as poss
-usually mix of salt + sugar. Hartmann’s v good most similar to normal physiology but only low amount of K+ and can’t give extra.
Correcting fluid deficit
Correct dehydration
If reduced UO fluid challenge of 250-500ml over 15-30mins, can give up to 2L then need senior help
Replacing ongoing fluid losses?
Check for third space losses, is there diuresis, tachypnoea/fever, high stoma output, diarrhoea, is fluid they are losing rich in electrolytes? So replace these as well as their normal daily requirements
Which electrolytes are lost in fluid losses?
Vomiting - Na+, H+, K+
Diarrhoea - Na+, K+, HCO3-
All GI secretions - lots of K+
What happens if you give RhD+ blood to a RhD- male?
RhD antigen - 85% have it (RhD+)
They will develop the RhD antibody, but not an issue as they don’t attack their own blood
But obv better to give matched blood
Why is RhD mismatch an issue in women?
RhD- mother + RhD+ father
Mother contracts RhD+ blood from foetus - develops antibodies - fine for first pregnancy
In second pregnancy, the mother’s anti-D antibodies cross the placenta and enter the foetus’ RhD+ blood
Antibody binds to RhD+ antigens - foetal immune system attacks + destroys its own RBCs - haemolytic disease of the newborn
How is haemolytic disease of the newborn prevented?
Give RhD specific blood to women when they need transfusions
Test during first pregnancy, if they are RhD - give injection of anti-RhD immunoglobulin around 28w, so foetal RhD+ RBCs get destroyed before mother exposed to + sensitised to them (which happens a bit later in pregnancy) - passive immunity
