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rinciples of



© Ogan Gurel, MD
Table of Contents

PREOP ................................................................................................................................................................... 1
Communication................................................................................................................................................ 2
Routine Preop preparations............................................................................................................................. 4
Preop rituals .................................................................................................................................................... 5
Pre-existing Cardiovascular Disease .............................................................................................................. 7
Pre-existing Respiratory Disease..................................................................................................................... 9
Pre-existing Gastrointestinal Disease ........................................................................................................... 11
Pre-existing Renal Disease ............................................................................................................................ 14
Pre-existing Hematologic Disease................................................................................................................. 15
Pre-existing Endocrinological Disease ......................................................................................................... 17
Pre-existing Neuromuscular Disease............................................................................................................. 20
Pre-existing Psychiatric Disease ................................................................................................................... 21
Miscellaneous pre-existing conditions........................................................................................................... 22
POSTOP ............................................................................................................................................................... 23
Acute Pain...................................................................................................................................................... 24
Pain Management: Pharmacology ................................................................................................................ 25
Simple Analgesic Techniques......................................................................................................................... 28
Advanced Analgesic Techniques.................................................................................................................... 30
Nausea & Vomiting........................................................................................................................................ 32
Fluids & Electrolyte Balance......................................................................................................................... 35
Bleeding & Transfusion ................................................................................................................................. 40
Feeding .......................................................................................................................................................... 44
Blood Gases ................................................................................................................................................... 46
Monitoring Devices........................................................................................................................................ 50
Hypotension ................................................................................................................................................... 52
Dysrhythmias ................................................................................................................................................. 56
Hypertension.................................................................................................................................................. 61
Myocardial Ischemia ..................................................................................................................................... 63
Pulmonary Edema ......................................................................................................................................... 65
Cardiac Arrest ............................................................................................................................................... 69
Respiratory Problems .................................................................................................................................... 72
Oliguria & Catheters ..................................................................................................................................... 81
Fever.............................................................................................................................................................. 84
Hypothermia .................................................................................................................................................. 87
CNS complications......................................................................................................................................... 89
Thrombosis .................................................................................................................................................... 95
Miscellaneous Postoperative problems ......................................................................................................... 97
Principles of Perioperative Care © Ogan Gurel, MD

A complete, systematic, open-minded H+P is important to

optimize patients for surgery
(and to optimize the surgery for the patient)

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 You will be judged more on your communications skills than on any other aspect
of your job

Talking to patients

 Learn patient’s names
 Introduce yourself
 Shake hands

Dress code
 Tie, avoid wearing scrubs, daily shave

Make time
 Avoid being curt
 Shake hands & sit down (for H+P)
 Make the purpose of the visit clear at the outset (“I’m here to place an IV, etc.)

 Essential

Dealing with complaints

 Apologize early (an apology is not an admission of liability)
 Explain circumstances truthfully
 Refer up the line to seniors

Talking to professionals

 Get senior residents involved early in developing problems
 Document your discussion with senior residents
 Call senior (and have attending contacted) whenever a major (especially an
unexpected) change in patient management occurs (e.g. an admission, discharge,
ICU transfer, consult, etc.)

Other Specialists
 Make personal visits when possible; (use beeps sparingly)
 Visit ICU patients at least once daily

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 When consulting other services ask for advice (not services)

 Document your discussions

 Send a brief note upon DC
 D-SUM include: nature of surgery, any complications, drug regimen and f/u
 With deaths call PCP

 Learn their names
 Treat them with respect
 Ask their advice

 Date and time (military)
 If you put plan of action at end of note be sure to follow-through
 If you talk to senior, be sure to record the fact
 Sign name (print last name & beeper number)

 Do not put DEA number on unscheduled drugs
 For scheduled drugs use a prime number (2, 3, 5, 7, 11, 13, 17, 19, 23, 29 , 31, 37,
41, 43, 47, 53, 59, 61, 67, 71 , 73, 79, 83, 89, 97, 101)
 Use generic names
 Put full-name, address, age & date
 Write Rx for OTC meds if there is a question of compliance

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Routine Preop preparations

 Confirm surgical lesion
 ROS (focus on CV & resp systems)
 Detailed drug history
 Allergies (always ask what happened)

Preoperative Investigations

Screening tests
 UA
 Lytes, BUN, Cr
 EKG (> 60, younger if smoker / major surgery)

Tests necessary due to pre-existing illness



T+C 2U

T+C 4U

T+C 6U

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Preop rituals
 NPO/IVF pMN (avoid solids/clrs up to 4h/2h)
 Do not withhold oral medications

Regular Medication
 Very few drugs interfere with anesthesia/surgery
 Exceptions:
1. insulin & OHAs
2. anticoagulants
3. lithium
 Definitely continue cardiac meds

Bowel Prep

DVT prophylaxis

Antibiotic prophylaxis

To reduce incidence of postop wound infection

 Biliary: cephalosporin or amoxicillin
 Colorectal: cephalosporin with metronidazole
 Vascular: cephalosporin or amoxicillin
 Amputation: Penicillin, metronidazole and cephalosporin
 Orthopedics: cephalosporin

To prevent endocarditis in susceptible individuals

 High risk: patients with prosthetic valves or previous BE
 Moderate risk: RHD, septal defects, patent ductus, MV prolapse, aortic sclerosis,
h/o RF and IVDA

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 Rx: Amoxicillin 3g po or 1g IV followed by 400mg 6h pOP (if allergic to

penicillin give clindamicin 300 mg po followed by 150 mg 6h pOP

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Pre-existing Cardiovascular Disease

 Uncontrolled hypertensives subject to surgery tend to exhibit grossly exaggerated
BP responses which can lead to strokes & MIs
 Poorly controlled HTN = DBP > 110 -> should be controlled before surgery
 For well controlled hypertensives maintain all antihypertensive medications
 preop EKG; evidence of LVH or “strain” suggests higher risk; Lytes, BUN, Cr if
patient is on diuretics.
 Hypertension is associated with ischemic heart disease


 Exercise tolerance is a sensitive measure of cardiac reserve.
 Ask about past history of MIs/hospital admissions & cardiac medication.
 ? Orthopnea/PND

 rest tachycardia, LE edema, JVD, basilar rales.

 EKG -> look for dysrhythmias, old MI & acute ischemia
 Echo -> gives more information about fitness of the heart to tolerate
GA/Surgery than any other test. Most important: EF which is the best predictor
of outcome after major surgery. EF <40% particularly bad.
 CBC -> lower than usual threshold for treating anemia

Valvular Heart Disease

 Key idea is to identify those patients with fixed cardiac output states: aortic
stenosis, mitral stenosis and constrictive pericarditis. These patients react poorly
to vasodilatation (anesthesia).
 Patients with prosthetic heart valves require heavy anticoagulation at all times +
antibiotic coverage

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Ischemic Heart Disease

Recent MI (< 6 months)

 Postpone elective, non-cancer surgery

Unstable angina (angina with has recently changed in frequency

or severity).
 Increased NTG consumption is a sensitive measure of this.

 Atrial fibrillation is the most common abnormality
 Ventricular rate in controlled AF should be 80; question the adequacy of
treatment if this is higher.
 Maintain all anti-dysrhythmics
 Beware of hypokalemia or changes in renal function in patients on digoxin.
Digoxin levels should be taken 6h after the dose is given.

 No particular precautions for patients with pacemakers; electrocautery risk very

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Pre-existing Respiratory Disease

Fitness for Surgery

 Exercise tolerance
 H/O of chronic bronchitis -> purulent sputum
 Check current meds (steroids, NSAIDS)
 Ask about prior admissions, home oxygen, history of smoking

 Cyanosis, wheeze, dyspnea at rest, right heart failure, clubbing or focal chest signs

 CBC (elevated white count in PNA)
 ABG (baseline for major surgery/severe disease)
 PFTs (severe disease to VC, FEV1 and response to bronchodilators)


(stopping for …
 12-24hr reduces need for carbon monoxide & nicotine elimination
 3-4 days improves ciliary activity
 1-2 weeks reduces sputum volume
 6 weeks reduces pulmonary and coronary vascular resistance and restores normal
pulmonary macrophage function

Preop preparation
 stop smoking. 48hr intensive PT for sputum retainers


Gauging severity:
 ask about EW visits, previous admissions, courses of steroids, ICU stays, and
limitation of activities. Severe asthmatics are rarely wheeze-free.

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 Maintain all regular medications
 Avoid using bronchospastic drugs: morphine, all NSAIDs and -blockers.
 Humidify oxygen, treat pain adequately and avoid creating anxiety
 Consider dose of inhaler on call to OR

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Pre-existing Gastrointestinal

 body mass index combines height & weight BMI 
height 2 (m 2 )
 Obesity = BMI > 28
 Morbid obesity = BMI > 35

Cardiovascular problems
 HTN, CHF, ischemia more common
 Take history of snoring, day-time drowsiness
 Raised bicarbonate indicates carbon dioxide retention and thus may be a
contraindication to postop oxygen

Respiratory problems
 Increased work of breathing
 prone to PNA
 Nursing: upright position, mobilization, early PT, oxygen at night

Gastrointestinal problems
 Hiatal hernias, GERD common.
 Continue H2-blockers or omeprazole / Prilosec perioperatively

Metabolic issues
 Screen for diabetes
 Temporary insulin dependence may be a possibility

Venous access
 Avoid IM injections (usually intra-adipose)
 If prolonged access required think central line

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 Lytes, BUN, Cr especially with diarrhea or vomiting
 Glucose -> chronic hypoglycemia
 EKG -> weakened cardiac muscle -> CHF/dysrhythmias
 CXR -> preop PNA more common due to immunocompromise/weakness.
Pulmonary edema/pleural effusions due to hypoalbuminemia
 LFT/clotting: hypoalbuminemia, hypoglobulinema, prolonged PT

 Prone to infection, poor healing, skin ulcers, hypothermia
 IM route is unreliable due to reduced muscle blood flow

Upper GI problems

Heartburn & Indigestion

 Continue (or start) H2 antagonists/omeprazole
 Avoid particular antacids (use sodium citrate instead)

Upper GI bleeding

Liver Problems

 Bilirubin (yellow pigment) function is to cause renal failure
 Albumin is a protein without which you get edema & ascites
 PT/INR is a measure of clotting which is impaired in liver disease
 Liver enzymes are not measures of liver function at all but of liver damage

Acute jaundice (liver function is OK)

 Renal failure in jaundice is caused by toxins & precipitated by hypovolemia;
hydrate -> 1ml/kg/hr
 Clotting is deranged (because vit K is fat-soluble and requires bile salts in the
intestine for absorption). Give vit K IM (wait 24hr). Otherwise give FFP 6U.
 Hypoxia (because of increased pulmonary shunt). Give postop oxygen; use sat
monitor & good analgesia.

Liver failure (leads to ascites, jaundice and encephalopathy)

 For clotting disorders use FFP (vit K is useless)
 Protect gastric mucosa (with H2-blockers or omeprazole)

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 For renal failure maintain diuresis

 Drug metabolism unpredictable; avoid sedatives and titrate analgesics in small IV
 To prevent encephalopathy order a low-protein diet; think of oral neomycin,
lactulose, and/or rectal magnesium sulfate.

Lower GI tract problems

 Results in hypovolemia, hyponatremia, hypokalemia and acidosis.
 Replace with NS with 20-40 K (depending on K results)
 Acidosis may be treated with bicarbonate

Bowel prep
 Iatrogenic hypovolemia is common
 Replace with 2 liters of NS over 24hr preoperatively

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Pre-existing Renal Disease

Chronic Renal Failure

Associated conditions

Medications in CRF

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Pre-existing Hematologic Disease

 Anemia is important because it increases the risk of perioperative ischemia. (Hb
< 12 in males, < 10 in females)
 Classify according to erythrocyte size & hemoglobin content

Microcytic, hypochromic
 MCV < 75
 Most commonly due to chronic blood loss
 More rarely due to failure to absorb or utilize iron
 Rx with oral ferrous sulfate (will raise Hb by 2 g/dl in 2 weeks)
 Transfusion will raise Hb by 1 g/dl per unit
 Ideally transfuse 2 days preop to give time for stored cells to return to normal
oxygen delivery
 Transfuse patients with history of ischemic heart disease more aggressively (keep
Hb > 10).

Normocytic, normochromic
 Anemia of chronic disease (renal failure, severe connective tissue disease and
 Do not require transfusion because anemia is well-compensated by increased
intracellular 2,3-DPG which stabilizes the deoxy state allow the hemoglobin to
release oxygen more readily in the tissues.
 Transfusion in renal failure may be harmful

Macrocytic (megaloblastic)
 MCV > 96.
 Result of either folate or B12 deficiencies due to diet, malabsorption or increased
demand (pregnancy).
 Associated with heart failure; transfuse only packed cells and consider using a
 Important to send blood for B12 and folate assays before treating with folate.
 Treat B12 deficits with hydroxocobalamin 1mg IM.

Bleeding Disorders
 Usually iatrogenic (rather than pathologic)

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 Warfarin / Coumadin therapy measured by INR (2-4.5) for DVT, valve
 DC warfarin 2-3 days preop and replace with heparin (if necessary)
 For urgent correction of coagulopathy treatment of choice is FFP (6U FFP = 1
 In catastrophic cases may also consider vit K (5mg slowly IV) but it is slow-
acting, makes later AC difficult, and there is also a risk of anaphylaxis.

 Short half-life (~1hour) means that effect can be reversed by stopping 3-4 hours
 Typical dose is 1000 U / hr which will achieve a 50% prolongation of PTT
 Check PTT at least qD
 When restarting warfarin it is necessary to overlap warfarin and heparin for 2-3

 Minimum acceptable count is 100,000
 Transfusing one unit will raise the platelet count by 5,000


Sickle cell anemia

 Screening test
 Preoperative transfusion may be necessary
 Tourniquets can precipitate sickling
 Postoperatively prevent a crisis: pain, cold, infection, acidosis and hypoxia are the
principal causes. Should a crisis occur, the risk of pulmonary embolus becomes
very high -> AC

 Polycythemia vera or secondary polycythemia
 PV patients should undergo venesection 1-2 days preop
 Secondary polycythemia due to increase erythropoeitin secondary to chronic
hypoxia. Full pulmonary work-up, possible venesection, and DVT prophylaxis

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Pre-existing Endocrinological
 Collective term for insulin deficiency states

Principles of Management

 All diabetics are at increased risk of MI, PVD and CVA. Careful PE & EKG.
 Ischemia is often occult

Infectious Disease
 Infection worsens diabetic control
 Diabetics are immunocompromised
 Consider preop Abx
 Rigid exclusion of URI/UTI important

 DM causes CRF
 Check Lytes, Bun, Cr preop

 Autonomic neuropathy can cause hypotension
 On exam:
1. Pulse rate does not change on Valsalva
2. Postural hypotension

Principles of Metabolic Control

 Hyperglycemia affects CNS only indirectly and slowly through acid-base and
electrolyte disturbance, while hypoglycemia leads to problems very rapidly

 Put early on for AM operations
 Stop long-acting OHAs at least 18h preop
 Check BS in AM and just before surgery
 If hypoglycemic put in D5W; if hyperglycemic do not start insulin

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 Omit long-acting insulins the night before; continue short-acting insulins for the
evening meal. Omit all insulins on the morning of surgery.
 DKA: hypovolemia, acidosis, hyponatremia and hyperglycemia. ICU admission.
Correct hypovolemia with saline (~2l/hr), give insulin bolus (20U) and replace
potassium (20 meq KCl per liter)

Thyroid problems


Preoperative testing
 TFTs; all cases should be euthyroid
 Surgery without medical control of hyperthyroidism risks “thyroid storm’.
Carbimazole and/or -blockers. Iodine sometimes given to reduce vascularity
 Indirect laryngoscopy (via ENT) to exclude a pre-existing laryngeal nerve palsy.
If the other normal nerve were to be injured -> b/l palsy which could threaten
the airway.
 CXR/thoracic inlet views/CT scan->tracheal compression, substernal
 Preoperative calcium for baseline. To compare to post-op calcium as indicator of
parathyroid injury

Postop considerations
 Airway obstruction due to hematoma, edema, nerve palsies or cartilage erosion -
> pair of scissors or staple removers at bedside
 Acute hypoparathyroidism. Check postop calcium and signs of tetany. IV
calcium gluconate 10% 10ml slowly.

 At risk of heart failure, hypothermia, over-sedation and pneumonia

Adrenocortical problems
 Addisonian crisis -> hypotension, hyponatremia, hyperkalemia.
 Resuscitate with IV steroids and saline.
 With chronic Addison’s measure preop lytes, glucose.
 Patients on long-term steroids (or previous steroid therapy within one year) need
stress steroids (hydrocortisone 100 mg IV at induction and 8 hr post-op x one
day). Does halved each day until preop dose is reached.
 Hydrocortisone (100 mg IV/IM) = Prednisolone (25mg PO).

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Diabetes insipidus
 May follow head injury or neurosurgery
 Due to failure of production or action of ADH resulting in large volumes of
dilute urine (specific gravity < 1.010).
 Treat with intranasal DDAVP (synthetic ADH) 10-40 mcg/day.

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Pre-existing Neuromuscular Disease

 Some AEDs can cause blood dyscrasias
 Do not discontinue any AEDs
 Phenothiazines [chlorpromazine/thorazine & prochlorperazine/compazine] lower
the seizure threshold

 Indication that there is underlying atherosclerosis or cardiac Dz -> preop EKG
 Swallowing difficult predisposes to malnutrition & aspiration PNA
 Immobility increases DVT risk & skin breakdown
 Higher risk of PNA & UTI
 Hypovolemia & hypoxia should be avoided

Parkinson’s disease
 Possible further respiratory compromise due to rigidity of the thorax.
 Continue anti-Parkinsonian drugs but watch for urinary retention + confusion
(anti-cholinergic effects).
 Central dopamine antagonists [droperidol/, haloperidol/haldol,
metoclopramide/reglan] may worsen disease.

Multiple Sclerosis
 Risk of UTI/PNA (aspiration) high.
 Autonomic hyper-reflexia (full bladder of constipation) may lead to uncontrolled
autonomic reflex with severe hypertension, sweating and bradycardia.
 Good catheter and bowel care.

Myasthenia gravis
 Do not withdraw anticholinesterases or steroids.

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Pre-existing Psychiatric Disease


 Sudden withdrawal manifests as a panic attack -> severe w/d -> Sz.
 Sx develop within a day to week (depending on half-life of drug).
 Continue usual medications.

 Side-effects of tricyclics include urinary retention, constipation, blood dyscrasias,
electrolyte imbalance, dysrhythmias and confusion.
 CBC, Lytes, EKG are needed preop
 SSRIs are safer than tricyclics but same studies needed.
 MAOIs. Do not discontinue. May not have sympathomimetics.

 such as the phenothiazines (thorazine) have many side effects: Parkinsonianism,
blood dyscrasias, urinary retention, constipation, hypotension and hypothermia.
 Effects are additive with other phenothiazines [prochlorperazine/compazine] or
other dopamine antagonists [metochlopramide/reglan].

 Narrow therapeutic window (0.4 - 1.0). Toxic effects may occur > 1.5.
 Toxicity: mixed cerebellar signs, confusion, coma, convulsions, diarrhea and
 Toxicity is precipitated by hyponatremia, dehydration, pyrexia and loop diuretics.
 Advisable to measure serum lithium preop

 Prevent withdrawal: alcohol or benzodiazepines
 Oral diazepam/valium 30mg in divided doses on first day and reduce by 5mg/day
until maintenance of 10mg/day is reached


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Miscellaneous pre-existing
 Risks to fetus are teratogenesis in the first trimester and premature labor in the
third trimester. Second trimester is the safest.
 After 16 weeks greater risk of aspiration -> H2 blocker/
 Resting respiratory rate and heart rate higher; BP lower. Greatly increased risk of
DVT/PE. Urine output and maintenance IVF requirements are higher.
 Compression of inferior vena cava -> place on left lateral decubitus position

Breast feeding
 Safe medications: morphine, acetaminophen, ibuprofen, metoclopramide and
 Do not give: aspirin (risk of Reye’s), atropine (anticholinergic effects), barbiturates
(drowsiness in high doses), chloramphenicol (bone marrow toxicity in the fetus),
ciprofloxacin (large concentrations in breast milk), tetracycline (possibility of
dental discoloration)

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Important to institute a servo-loop approach to patient

management: assess, therapy, reassess, adjust therapy, etc.

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Acute Pain
What is the problem
 Pain control is poorly managed
 It is important to identify causes of pain that need a different form of
intervention (i.e. an operation).

Consequences of pain
 Psychological
 Secondary psychological
 Respiratory
 Cardiovascular
 Other

Pain measurement
 1-10 pain score
 Important to use a series of pain scores to assess titration of therapy with response
with frequent assessment

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Pain Management: Pharmacology

 All opioids cause analgesia, N/V and respiratory depression


 there is no such thing as more potent opioid ... just different dosages

Nausea & Vomiting

 Nausea & vomiting is common: write for anti-emetic Rx

Respiratory Depression
 Assess by RR (< 8 is bad).
 Never use a pulse oximeter (hypoxia is a late sign).
 Respiratory depression is accompanied by somnolence.
 Management of respiratory depression with naloxone / Narcan (0.2 mg IV).
Short duration of action (~10 min) so repeated doses may be required.

 Patients given opioids appropriately when in acute pain do NOT become
 Dose requirements vary enormously ... depending on severity of pain, age, prior
opioid use, psychological factors and weight.


 Fast onset; duration 4-6 hours. Side-effects include delayed gastric emptying,
constipation, spasm of sphincter of Oddi. Histamine release which may cause
bronchospasm in asthmatics. Typical IM dose is 10mg q3 PRN

 Less spasm of sphincter of Oddi

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Mode of action
 Analgesic, antipyretic and anti-inflammatory actions
 Mode of action (peripheral inhibition of prostaglandin synthesis) is completely
separate from opioids so are safe to use in combination
 Very effective in postoperative pain relief ... so should be used in every case
where contraindications do not exist

Side effects

Gastric irritation
 Hazard whatever the route of administration
 Contraindicated in patients with GU/DU or predisposition to UGIB
 Always prescribe NSAIDs to be taken with food

Renal effects
 Reduction in blood flow, sodium & water retention
 Use with caution in anyone with renal disease, hypovolemia, hypertension or gout
 Check chemistries frequently

Platelet inhibition
 Only becomes a postoperative problem with patients with thrombocytopenia,
dysfunctional platelets or large raw areas to bleed from.

 Avoid NSAIDs in asthmatics or those with nasal polyps
 strongly contraindicated in the presence of active bronchospasm

Drug interactions
 Increase in anticoagulation during warfarin therapy

Specific Drugs

 Doses 500-1000 mg q 4-6hr
 Absolutely contraindicated for children

Ibuprofen / Motrin
 Dose 200-400 mg q4-8hr
 Causes fewer side-effects than aspirin

Ketorolac / Toradol
 Powerful ... equivalent to 10mg of MS
 IM form

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Combination pills
 Very low risk of side-effects and high efficacy

Role of sedatives
 Benzodiazepines have a weak muscle relaxant action which may improve pain
associated with skeletal muscle contraction.
 Anxiolytic effects may be useful but only if anxiety is a major component of the
pain state.
 Treat pain with analgesics, not sedatives

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Simple Analgesic Techniques

Non-drug analgesia
 Talk with patient
 Appropriate use of traction/splinting etc.

Enteral therapy
 Preferred route
 Bioavailability is often less than parenteral routes
 Meds per NGT require a liquid preparation

IM therapy
 Use in patients who have moderate pain and who are expected to rapidly
progress to oral pain medications

 PRN basis … which is bad
 IM therapy is time-consuming and labor-intensive
 IM injections hurt … patients thus avoid them
 Can result in excessive peaks & troughs
 Variable absorption … contraindicated with patients in shock
 Also contraindicated in patients with coagulopathy

PRN vs. RTC medication

 Try to have a regular element to any pain prescription with a PRN rescue
 Or … write RTC unless refused by patient

Loading doses
 Importance of loading doses
 Loading doses are given IV
 Use an assessment-therapy-reassessment servo loop
 Start with 2 mg MS

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 Have an amp of naloxone (0.4 mg) ready.

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Advanced Analgesic Techniques

 Safe and effective
 Concentration, demand dose, lockout interval, basal rate
 Basal rate usually does not improve the quality of the analgesia but increases the
incidence of side-effects


 Local anesthetic
 Opioids
 Combination of opioid (fentanyl) + weak anesthetic (0.125% bupivicaine)
 Useful for thoracotomy, major laparotomy, multiple rib Fx, high risk patients,
cancer pain & terminal care

Adverse Effects
 Respiratory depression
 Hypotension -> Rx with fluid bolus
 Pruritis -> chlorpheniramine (10 - 20 mg IM) or decrease rate of infusion
 Urinary retention
 Nausea
 Sedation -> reduce rate
 Motor or sensory block -> reassurance

Special circumstances

Respiratory disease
 Pain is definitely more dangerous than analgesia

CNS depression

 Shock should be treated before analgesia is given
 Fentanyl IV in increments of 25 - 50 mcg

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 Do not give IM drugs of any kind to a shocked patient

Narcotic addiction
 Get advice from pain specialist


Neurogenic pain
 Does not respond to opioids
 Often lancinating (shooting or electric)
 Treatment may include carbamazepine/Tegretol, amitriptyline/Elavil, baclofen,
nerve blocks, neurosurgery

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Nausea & Vomiting

Physiology of emesis
 Vomiting is a reflex involving:
1. emetic detectors,
2. central integrating area, and
3. motor outputs
 Four emetic areas:
4. CTZ
5. Vestibular system
6. Gastrointestinal afferents
7. Higher centers

Causes of emesis

Preoperative factors
 Raised ICP
 Bowel obstruction

Direct drug actions

 Opioid receptors in the CTZ
 Opioid receptors also delay gastric emptying
 Opioids sensitize the emetic response to labyrinthine stimuli
 Opioids enhance serotonin release in the gut

Indirect drug effects

 GI effects: some anesthetics reduce GI motility or inhalational agents may diffuse
to gut causing distention
 CV effects: hypotension (as with spinals) may precipitate N/V
 CNS effects: drug-induced increased ICP may worsen nausea

Patient factors: increased risk with

 Patients who have motion sickness
 Previous pOP N/V
 Females > males
 Anxiety -> orophagia and delayed gastric emptying
 obesity

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Effects of the surgery

 Intrabdominal surgery
 Laparoscopic gyn surgery
 ear surgery
 T&A

Surgical complications
 Ileus
 bowel obstruction
 pancreatitis
 Myocardial infarction (especially inferior ) may cause N/V

Complications of emesis

Fluid & electrolyte loss

 Hypokalemia
 Alkalosis

Physical effects
 Wound dehiscence
 Mallory-Weiss tear -> esophageal rupture

Physiological effects
 Hypertension & tachycardia -> myocardial infarction, CVA


General measures
 Placement of NGT

Phenothiazines (like chlorpromazine / thorazine)

 Prochlorperazine/Compazine
 The most useful agents (block dopamine receptors on CTZ)
 Extra-pyramidal side-effects (0.3% incidence) … very low with doses < 10 mg
 Other effects include sedation, hypotension, cholestatic jaundice, skin sensitivity
and hyperprolactinemia

Butyrophenones (like haloperidol / haldol)

 Droperidol
 Effect is less striking than with phenothiazines
 Hypotension can occur due to -blockade
 About 20% of patients complain later of a generalized feeling of malaise and

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GI prokinetic agents
 Metoclopramide/Reglan
 Increases motility of the GI tract, blocks dopamine receptors at the CTZ
 Works poorly however.

5-HT3 antagonists
 Ondansetron/Zofran
 Used in N/V of chemotherapy

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Fluids & Electrolyte Balance

Normal maintenance
requirements Total body water
Cell memb
 Potassium intracellular ECF Capillary
 Sodium extracellular Plasma
 Water 30 ml/kg/day ->
~ 2000 cc/day
 Sodium 1-2 meq/kg/day -> ~ 60 - 120 meq / day
 Potassium 1 meq/kg/day -> ~ 60 meq /day

Deficits and losses

Normal losses
 UO 1500 cc/day.
 Insensible losses 0.5 cc/kg/hr.
 Fever, obesity increase insensible losses.

Special surgical losses

 EBL.
 Third space (injury causes increased local capillary permeability).

Other measured losses

 Significant volumes should be recorded and replaced.
 Diarrhea -> very large potassium losses (30 -70 meq/l).

Pre-existing deficits

Stress & Fluid balance

 Stress response -> increased aldosterone & ADH
 Stressed patients therefore cannot excrete large water loads
 ADH increases cannot be modified so use of hypotonic solutions is not

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 Crystalloid (small particles)
 Colloid (large molecules capable of exerting oncotic pressure)

 Distribution of IVF depends primarily on sodium content
 NS/LR -> freely distributed in extracellular compartment
 D5 (sugar gets pulled into cells) thus it is like giving pure water. Distributes in
the total body water
 D5/saline; 20% stays in ECF, majority ends up in total body water.

 Retained within intravascular space
 With shock and injury (increase in capillary permeability) colloid molecules reach
the interstitial space thus worsening edema


 Ask about thirst, prolonged vomiting/diarrhea
 Drowsiness, headaches, dizziness, malaise, delayed mobilization

 Consider all information not charted: prior deficits, insensible loss, third space
loss, internal hemorrhage
 UO 0.5 - 1ml /kg /hr. Oliguria is most commonly caused by inadequate volume,
but renal impairment and urinary obstruction must be ruled out

 Dry mucous membranes
 Edema
 Pulse rate/pressure
 warm/cold extremities
 Rales
 Skin turgor
 Daily weights

 Serial measurements of CVP
 Hematocrit may point to hemorrhage ... may take several hours
 Increased BUN in dehydration
 CXR -> pulmonary edema indicating overhydration

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Requirement = Pre - existing deficit

Planning a regimen
+ normal maintenance
 Aim is to produce a stable but + ongoing losses
slightly dry patient

Pre-existing deficit
 Treat there and then with a fluid challenge servo loop (give 250 cc NS and
reassess HD/UO.
 Do not “speed up the drip” and leave

 500 ml NS
 1500 ml D5

Ongoing Losses
 Usually sodium - containing so replete with D5NS, NS or LR
 Potassium (20 - 40 meq/l)
 Blood (keep Hct > 30)
 GI losses (give NS with 20meq/l KCl); large losses should have electrolyte
content measured to ensure appropriate replacement
 Nutrition
 Check daily chemistries while on IV fluids

Special situations

Cardiac failure
 Heart failure does not affect the rate of fluid loss so maintenance
fluid/electrolyte requirements are the same
 But ... cannot cope with as wide a range of filling pressures so aggressive fluid
resuscitation should only be used with good evidence of ECF loss/deficit.
 Continue diuretics
 Changes in physical signs are important

Respiratory disease
 Small and clinically undetectable degrees of fluid overload can dramatically
worsen pulmonary function.
 Better to err on the dry side

Liver disease
 Obstructive jaundice at risk of hepatorenal syndrome ... maintain high UO
 Decrease sodium intake

Renal disease
 Strict I/Os; daily chemistries

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 Err on the wet side .. nothing will finish off a failing kidney quicker than
 Avoid potentially nephrotoxic drugs ... NSAIDs, aminoglycosides, loop diuretics

 May be severely dehydrated on presentation
 Renal impairment common

Other problems

Septic Shock
 Often huge volumes are required

 Repeated bolus fluid resuscitation may be required as hypothermic patient warms

Hormone problems

Electrolyte disturbances

 K < 3.5
 Symptoms of muscle weakness
 Causes include excessive K loss (diarrhea, vomiting), inadequate replacement,
alkalosis/hyperventilation, diuretic therapy
 Requirements 60 meq/day

 K > 5.0
 Acute changes more serious than chronic
 Causes: renal failure, acidosis, hypercatabolism (malignant hypothermia)

 10% Ca-Gluconate
 Correct acidosis
 Dextrose / Insulin (50 ml D50 with 20 units insulin over 30 minutes)
 Kayexelate 30mg tid po/pr
 Arrange dialysis

 A sign of excess water
 Causes: iatrogenic (hypotonic IVF), TUR syndrome, SIADH
 Acute dilutional: water restriction
 Acute salt-losing resuscitate with NS+K

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 Diuretic-induced

 Due to lack of water
 Fluid resuscitate with D5 or D5NS

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Bleeding & Transfusion

Diagnosis of bleeding
 Heart rate: Tachycardia (loss > 15%); ST -> 120 (>30%)
 Blood pressure decreases late (> 30% blood volume); an earlier change is
decrease in pulse pressure
 Urine output < 0.5 ml/kg/hr represents a 30% loss
 Level of consciousness 15% -> anxiety, 30% to confusion, 40% to lethargy or
 Respiratory rate increases (? due to physiological dead space)
 Skin signs pallor, poor capillary refill (normally < 1 sec) and reduced skin turgor
 CVP/JVP more important as relative measures (compensatory venoconstriction
may misleadingly increase CVP)
 Hematocrit does not decrease acutely but only after dilution; only makes sense
with a separate assessment of volume status


Surgical lesions
 Most common reason is lack of hemostasis
 A dry drain does not exclude bleeding

Bleeding disorders

 Dilution of platelets/clotting factors
 Inhibition of platelets/clotting factors
 Consumption of platelets/clotting factors by DIC/cardiopulmonary bypass

 Diagnosis is a clinical one: bleeding at venipuncture sites, bruises, bleeding
mucosa, hematuria, hemarthroses. Labs are used to define cause & guide therapy
 PT: Warfarin, dilution, DIC or liver disease prolong PT
 PTT: dilution, DIC or heparin
 LFTs liver is major source of clotting factors
 FDPs fibrin degradation products seen with DIC
 Chemistries: urea is a platelet inhibitor
 Ionized calcium: hypocalcemia is a rare cause of coagulopathy. Tourniquet falsely
elevates serum calcium. Best assay is the ionized calcium

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Principles of treatment

Preventing further hemorrhage

 Elevation (especially for venous bleeding)
 Direct pressure

Supportive treatment

Causes of death
 hypovolemia (1st priority)
 loss of oxygen transporting capability

Restore plasma volume

 crystalloid useful (but only 30% stays in circulation)
 colloid require less volume
 blood products to restore both volume and oxygen carriage
 Inotropes are not used

Restore oxygen carriage

 Oxygen
 Hb > 10 g/dl
 500 ml blood loss -> 1g/dl drop in hemoglobin

Definitive treatment
 Usually exploratory surgery

Bleeding in children

Physiological differences
 Faster HR
 Lower SBP
 Higher RR
 Higher UO (1ml/kg/hr)

Volume calculations
 Simplest measure is weight
 8% of body weight is blood
 First fluid bolus is 20 ml/kg of salt

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Red cell transfusions

 Two indications: acute hemorrhage & anemia
 As much as possible, anemia should be treated with hematinics (iron, folate, vit
B12). Decision to transfuse: Hct, expectation of further blood loss, patient’s
general health (especially cardiac patients).
 Patients with renal failure should generally not be transfused (problems with fluid
 > 18 gauge IV
 Furosemide / Lasix only rarely indicated
 Avoid transfusing o/n (because of need for frequent VS checks)
 One unit of blood will increase Hb / Hct by 1 / 3.

Plasma products
 FFP -> replacement of clotting factors
 Indications
1. Massive transfusion
2. Rapid correction of warfarin / Coumadin anticoagulation
 Ask for 2 U FFP whenever you ask for 4 or more units of PRBC

 Depends on platelet count.
 Tx for platelets < 50,000

Preoperative cross-matching


Complications of blood transfusion

Fluid overload
 Elderly, known cardiac disease and megaloblastic anemia
 Treat chronic anemia with PRBCs & give it slowly
 Concomitant diuretic (furosemide / Lasix 20mg PO) with every other unit of


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Immunological complications

ABO incompatibility

Rh incompatibility & other antibodies

Other reactions
 Coagulopathy (since stored blood contains very little clotting factors)
 Hypothermia
 Citrate toxicity -> hypocalcemia & acidosis
 Hyperkalemia
 Impaired oxygen delivery (stored blood progressively loses 2,3-DPG)

Other complications

Jehovah’s Witnesses

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The effects of starvation
 Liver -> 24 hr of glucose
 Afterwards glucose from gluconeogenesis (from AA)
 Decrease in BMR
 Negative nitrogen balance which can be reversed in simple starvation but not in
starvation accompanied by stress

The stress response

 Catecholamines, glucocorticoids, growth hormone, glucagon causing increased
protein catabolism, accelerated gluconeogenesis & insulin resistance
 Aldosterone & ADH cause salt and water retention

Enteral nutrition
 Use the gut if functional
 If swallowing not possible or low PO intake use NGT (or feeding tube); check
with CXR -> below diaphragm
 For long-term feeding G-tube or J-tube
 If slow gastric emptying -> cisapride/Propulsid 10 mg po tid or metoclopramide /
reglan 10 mg po tid
 Complications of TFs: diarrhea, tube insertion, pulmonary aspiration (tube
promotes regurgitation)
 Begin with low-strength ‘starter’ solution then proceed to full strength
 Decrease diarrhea but reduce rate of infusion, switch to iso-osmolar solution,
treat with codeine or loperamide/Lomotil)

Parenteral nutrition
 Gut dysfunction; contraindicated when gut feeding is possible
 Give through central line; nothing else in line due to infection risk

Choice of regimen
 Daily regimen

 VS/fluid balance

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 LFTs, chemistries, CPM, lipids, UA

 Catheter complications
 Sepsis (C-reactive protein is a sensitive marker of line infection)
 Fluid overload (esp. cardiac/renal/elderly patient)
 Hyperglycemia
 Electrolyte imbalance
 Trace element deficiency
 Carbon dioxide production

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Blood Gases
Acid-base physiology
 Maintenance of pH is essential
 H+ is constantly produced by the body as a product of metabolism.
 Buffer systems attenuate fluctuations in pH by reducing the free H+
 Most important buffer is the bicarbonate system
H   HCO3  H 2 CO3  H 2 O  CO2
produced by metabolism buffer removed by ventilation

 Acid can be removed via three process:

1. Immediate taken up by bicarbonate
2. Short-term via removal of CO2
3. Long-term (definitive) via kidney & gut
 Two groups of disturbances:
Metabolic (production or excretion of acid)
Respiratory (problem with excretion of CO2)

Control mechanisms
 Recall the Henderson-Hasselbach equation:

[ HCO3  ]
pH  pK  log
[CO2 ]
 pH depends on the balance between bicarbonate and carbon dioxide
 Whenever a physiological pH is perturbed, the body will attempt to compensate
for the abnormality
 Short-term compensation (minutes) via respiratory system
 Long-term compensation (days) via renal system
 The body never over-compensates for an acid-base disturbance

Blood gas measurements

 pH most important: tells you whether you have an acidosis or alkalosis.
Normal range is 7.35 - 7.45.
 pCO2 tells you about alveolar ventilation, e.g. hyperventilation or
hypoventilation. Normal is 35 - 45 mm Hg
 pO2 tells you about oxygenation.

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 Basically two components: oxygenation & acid-base status

 Normal range for RA is 80 - 100 mmHg; pO2 drops with age
 FIO2. You need to interpret oxygenation in the context of the inspired oxygen
 Oxygen saturation. Unless the oxygen saturation is directly measured ... trust the
pulse oximeter result

Acid-base status
 Look at the pH and decide whether the changes are opposite to the pH or not.
1. Is it acidosis or alkalosis
2. Is the patient hyperventilating or hypoventilating?

Arterial vs. Venous sample

 Normal venous O2 is 40 mmHg and the normal saturation 75%
 If PaO2 is much more than 50 mmHg then it is unlikely to be venous.
 If the pulse oximeter saturation is substantially greater than the blood gas result
than the sample is unlikely to be arterial
 If any doubt, repeat the sample

Management of abnormalities

Metabolic acidosis

 Failure to excrete acid: renal failure
 Excessive production of acid: shock, post-MI, ketoacidosis

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 Excessive loss of bicarbonate: duodenal fistulae

 Excessive absorption of bicarbonate

 Directed at the cause

Bicarbonate for metabolic acidosis

 Commonest cause for acidosis is shock. Giving bicarbonate yields CO2 which
cannot be released because of poor tissue perfusion. CO2 enters the cells an
decreases the intracellular pH, thus aggravating the acidosis.
 Metabolic acidosis without tissue hypoxia is an indication for bicarbonate
Bicarb(mmol )  base deficit  0.3  body wt (kg)
 Give half the calculated requirement over an hour first, then re-check gases. For
renal failure with fluid overload do dialysis.

Respiratory acidosis
 May be acute or chronic, or (acute-on-chronic … some with COPD who
 Acute respiratory acidosis is always serious … get senior assistance.
 Chronic may be subjected to “hypoxic drive” and may become apneic when
administered oxygen.

Causes of acute respiratory acidosis

 Respiratory depression
 Respiratory failure

Metabolic alkalosis

 Excessive bicarbonate administration
 Chronic potassium loss
 Pyloric stenosis (loss of acid without loss of bicarbonate) -> hypochloremic

 Give sodium & water to correct dehydration
 Give chloride to correct the deficit
 Give potassium
 NS with 40 meq /l KCl

Respiratory alkalosis
 Hyperventilation is the only cause
 Lung diseases (such as asthma, pneumonia, pulmonary fibrosis, mild pulmonary
 Anxiety which can lead to relative hypocalcemia (numbness & tingling in the
fingers, even tetany & spasm). Alkalosis deprotonates carboxyl groups on

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albumin making more sites available for binding to calcium. Treatment: breathe
in and out of a paper bag.

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Monitoring Devices
 Monitoring should never be a substitute for clinical judgment

Non-invasive blood pressure

 Pressure in various vessels varies as a result of presence of vessel disease
 Dimensions of cuff relative to arm are important
 Narrow cuff on a fat arm will overestimate the BP and an excessively narrow cuff
may lead to an underestimate.

Automated BP machines
 Oscillometry
 Onset of pulsations = SBP
 Point at which oscillations are the greatest = MAP
 Disappearance of pulsations = DBP

Arterial lines
 Only used in an ICU
 Used for continuous BP monitoring & blood sampling
 Most important dangers are exsanguination & intra-arterial injection

Central venous pressure monitoring

 Subclavian/IJ or femoral approaches; External jugular vein will not give reliable
reading on account of valve at proximal end
 Major complications: hemorrhage, pneumothorax and air embolus.
 Measurements of CVP should be taken at the end of expiration
 Reference point is the anterior axillary line in the 4th interspace
 Used as an estimate of volume status

Pulse oximeters

 oxyhemoglobin & deoxyhemoglobin have different optical absorption spectra.
 By passing two different wavelengths and measuring the relative absorption, the
proportion of oxygenated and deoxygenated blood can be estimated.

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 Poor signal (w/ poor perfusion)
 Other forms of hemoglobin. Carboxyhemoglobin & methemoglobin are similar
to oxyhemoglobin
 Dyes (bilirubin, methylene blue or nail varnish) will affect the reading
 Ambient light (strong light sources confuse the photocell)
 Venous pulsation (patients in cardiac failure, tricuspid regurgitation) may have
detectable venous pulsations

 Pulse oximeter should never be used as a means of detecting airway obstruction.
As the hemoglobin saturation falls, the warning will come far too late.
 Is not sensitive to hypoventilation if the patient is breathing oxygen.
 In comparing calculated (ABG) sats with pulse oximeter sats use the latter as it is
a measurement (unless the ABG has co-oximetry)

EKG monitoring
 Detection of dysrhythmias and ischemia
 For any unstable patient who you feel warrants closer monitoring use a pulse
oximeter and a Dinamap.

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 SBP < 90mmHg or significant drop (> 30 mmHg from recorded baseline)
 Evidence of end-organ dysfunction, e.g. low UO, decreased LOC


 Poor cardiac output secondary to decreased preload

 Pump problem due to poor myocardial contractility,

Septic / Anaphylactic
 Probably due to release of endotoxin from bacteria
 Early phase warm sepsis which proceeds to hypotension and cool extremities.
 Strongly associated with MSOF with a high mortality
 Anaphylactic shock is caused by a type I hypersensitivity reaction leading to
massive release of vasoactive mediators such as histamine

 Spinal shock

Combined causes
 pOP CHF may also be hypovolemic
 Early sepsis there is relative hypovolemia and in more advanced sepsis there is
direct myocardial depression

Other causes
 Drugs -> anesthetics, analgesics, antihypertensives
 Spinal/epidural anesthesia: due to autonomic blockade
 Vasovagal responses
 Drug toxicity: digoxin / Lanoxin, tricyclics, lithium
 Pulmonary embolus
 Measurement error
 Pregnancy: caval compression in late pregnancy. Heavily pregnant women
should not lie flat
 Hypothermia

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 Metabolic disorders; acidosis, disorders of calcium/phosphate, citrate toxicity

 Addisonian crisis: a patient with undiagnosed Addison’s or a patient who abruptly
stops taking steroids
 TUR syndrome: associate with hyponatremia following TURP

 Aimed at deciding the cause and severity of hypotension
 Airway: Talk to the patient. If the patient is speaking then the airway is clear.
 Breathing Check breath sounds. Give oxygen. Check RR
 Circulation Is there a pulse. Rate & character. Is the hypotension severe or
 Level of consciousness Awake & alert or comatose?
 If you have determined that a cardiac arrest is not imminent, then you can revert
to a more detailed assessment

 Age. PMH.
 Surgical diagnosis - any reason for active bleeding?
 Fluid history
 Onset of hypotension sudden or gradual?
 Recently administered drugs, especially pain medications
 Any specific symptoms? CP, SOB, itchy rash?

 Gen: Pallor, cyanosis; visible blood loss from drains/wounds, skin turgor.
Sweating, warm/cold extremities
 VS: pulse, measure BP manually, RR
 CV: JVP raised? Murmurs
 Chest: Lungs clear?
 Abd:

 UO (insert catheter if necessary
 Lytes, BUN, Cr
 EKG/CXR if suspicious of cardiogenic component

Central venous pressure monitoring

 Via central vein (subclavian, IJ or femoral) … not external jugular

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 Complications: hemorrhage, pneumothorax, air embolism

 Always get CXR after CVL insertion


Starling hypothesis
 Contractility is a function of initial fiber length
 Stroke volume varies with EDV
 EDV varies with volume status
 EDP varies with EDV
 Right EDP varies with left EDP. True in the healthy heart … however a variety
of conditions lead to a difference in function between the two sides of the heart
including respiratory disease, mitral stenosis, cardiac failure and pregnancy.
 CVP is the same as EDP

 Normal CVP is ~ 5 cm H2O
 CVP is a very indirect way of guessing left ventricular filling. Therefore absolute
values are meaningless. Do not base fluid management decisions on a single
CVP reading.
 Normal CVP does not rule out hypovolemia or fluid overload
 For patients with heart failure, there is a level of CVP which is optimal. This
“optimum” CVP is very unlikely to be within the “normal range”
 CVP is extremely useful when monitoring trends or response to treatment.


Basic resuscitation
 Airway
 Oxygen
 Large-bore IV

Fluid Challenge

 Once basic measures have been taken the cornerstone of treatment is the fluid
 The principle of the fluid challenge is an example of a servo loop.

 Infuse 100 - 200 ml of fluid rapidly and monitor the effects on heart rate, blood
pressure, UO and CVP.
 Crystalloid vs. Colloid is not important; however, D5 or D5½NS are not
particularly useful as their effect on ECF and intravascular volume is much less.

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 If the fluid therapy is indicated, then a favorable effect on the hemodynamic

variables will be seen and further challenges given. If deterioration, then
hypovolemia is unlikely to be present

 Never diagnose “fluid overload” purely on the basis of a fluid balance chart.
Many important loss never get charted.
 Do not base decisions on a single CVP reading
 The management of hemorrhage is surgical
 Blood should always be warmed when given rapidly
 Opioids are only rarely the sole cause of hypotension. However, when a
hypovolemic patient is given MS for pain, the blood pressure may drop
dramatically. The treatment is fluid, not naloxone / Narcan.

When the fluid challenge works

 Check hemodynamic variables: pulse, BP, UO, CVP.
 Repeat fluid boluses to rectify the situation. However, at each stage, the patient
should be re-assessed. Fluid overload, particularly in the elderly is a hazard if
fluid is given without regular assessment.

When the fluid challenge doesn’t work

 When the patient is in true cardiogenic shock. Invasive monitoring, inotrope
therapy, treatment of dysrhythmias.
 Different etiology such as tension pneumothorax, cardiac tamponade or
Addisonian crisis.
 Profound hypovolemia such that a small fluid challenge is inadequate to make a
noticeable difference.

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Immediate action
 Most commonly the result of pre-existing cardiac disease, but may occur as a
result of other factors such as hypoxia, hypovolemia, drug actions, electrolyte or
acid-base disturbances or a combination of these.
 Ensure the ABCs: airway, oxygen, breathing, pulse, BP, consciousness level.
Hypotension in the presence of dysrhythmia is an indication for urgent, expert
 Get a 12-lead EKG; get preop one for comparison and attempt a diagnosis
 Exclude any underlying causes: give oxygen, establish IV access and send Lytes,
BUN, Cr and blood gases
 Treat the dysrhythmia with specific therapy … or get someone to do it for you.

 Three simple things to decide:
 Is it tachycardia or bradycardia?
 Is it broad-complex QRS (> 0.12 sec or three small squares) or narrow-complex?
 Is it irregular or regular?

Atrial ectopic beats

 Extra beats on a background of sinus rhythm. QRS complexes are the same and
the P waves are different.

 Can be precipitated by caffeine, alcohol or stress although occasionally a more
sinister underlying cause such as electrolyte abnormality or drug toxicity (e.g.

 Treatment is usually not necessary.

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Ventricular ectopic beats

 Extra beats on a background of sinus rhythm, where the QRS complexes are
different from normal beats. The QRS complexes are wide and bizarre, and not
preceded by a P wave. They may be unifocal (where the abnormal QRS is always
the same) or multifocal, where they are different
 Must be taken seriously if they are:
1. Frequent (> 5/min)
2. Multifocal
3. Occurring in runs of two or more
4. Occurring at or just before the T wave, the so-called R-on-T
phenomenon, which can precipitate ventricular fibrillation

 If serious, An underlying cause such as electrolyte disturbance, ischemia or
hypoxia should be sought.

 Treatment is usually lidocaine 80 - 100 mg IV

Atrial fibrillation

 Irregular, usually narrow-complex tachycardia with absent P waves. Most
common dysrhythmia

 Long-standing AF is common in surgical patients.
 Acute AF can occur in myocardial infarction, thyrotoxicosis, pulmonary
embolism, electrolyte disturbances and hypoxia.
 A lapse in the patient’s regular digoxin dose may also cause new acute AF in the
previously well-controlled patient.

 Treat pain, hypovolemia, hypoxia
 For an undigitalized patient, a full loading dose of digoxin can be given IV
 For a digitalized patient, the usual problem is inadequate levels of digoxin and a
single extra dose (.5 mg orally will do the trick. Digoxin toxicity is possible,
particularly in the presence of hypokalemia.
 For a shocked patient use DC cardioversion
 Digoxin has a narrow therapeutic window, but undertreatment is more common
than toxicity. Almost nobody on 0.0625 or 0.125 mg qd has levels in the
therapeutic range (except for CRF patients). Loading dose is unchanged.

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Paroxysmal atrial fibrillation

 Flip in and out of AF. Digoxin will not prevent paroxysms of AF, but will
reduce the ventricular response.

 The drug of choice is sotalol 120 - 240 mg/day.

Supraventricular tachycardia

 Paroxysmal re-entrant tachycardia which on an EKG is a regular, narrow-
complex tachycardia with a rate usually between 140 and 250 bpm.
 Abnormal P waves with a fixed relationship to the QRS complex.

 Uncommon in postoperative period but may be seen in otherwise healthy young
patients who may have a history of palpitations. May occur after MI

 May respond to physiological measures which terminate the dysrhythmia by
provoking vagal activity. These include sustained valsalva maneuver or carotid
sinus massage.
 Valsalva … blow into manometer of a sphygmomanometer and asked to
maintain a pressure of 20-30 mmHg for 10 sec and then breath out. On
exhalation, there is a burst of vagal activity that slows conduction in the AV
node, and may terminate the dysrhythmia.
 Drug treatment: adenosine 6 mg IV followed by 6 mg, then 12 mg if necessary.
Adenosine is a powerful vasodilator, and transient hypotension is common.

Atrial flutter

 Flutter waves occur instead of P waves usually a rate of 300/min and give a
sawtooth appearance to the baseline. Normally there is a 2:1 or 3:1 block. A
narrow-complex tachycardia at a rate very close to 150 bpm is highly suggestive
of flutter with 2:1 block


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 Same management as for atrial fibrillation but primarily aimed at controlling the
ventricular rate, although amiodarone or DC cardioversion may restore sinus

Ventricular tachycardia
 Ventricular tachycardia is a medical emergency

 Any broad-complex tachycardia is VT until proven otherwise.
 The main diagnostic difficulty occurs with other forms of tachycardia in patients
who normally have BBB, and whose QRS complexes are always wide.
 Get 12-lead EKG and compare with previous traces.
 The diagnosis can be confirmed if independent atrial activity can be spotted:
regular P waves superimposed on the ventricular activity.

 Conscious patient: lidocaine 100mg (10 ml of 1%) followed by an infusion of 1-4
 Unconscious patients: same treatment as with VF


 Slow heart rate

 May be normal finding in fit individuals or during sleep as well as with patients
on -blockers.
 May also be an ominous sign, particularly of hypoxia.

 If no underlying cause then treat with oxygen and atropine (0.5 mg IV)

Heart Block

 1st degree: impulse is delayed but gets through each time. A sign of cardiac
disease but not an urgent problem.
 2nd degree: impulses are sometimes transmitted but not always. There are more P
waves than QRS complexes. There are two subtypes: type I in which the PR
interval gets progressively longer until a beat is dropped (the Wenckebach

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phenomenon) and the more serious type II in which the ratio of Ps to QRSs is
more fixed (e.g. occurring in 2:1 or 3:1 pattern). 2nd degree heart block deserves
urgent attention from a physician.
 3rd degree in which none of the atrial impulses are conducted. P waves are
regular but bear no relationship to the QRS complexes. The ventricular rate is
usually low. Occurs after MI, a result of degenerative changes in the conducting
system, or congenital

 Problem with conduction of the impulse between atria and ventricles.
 Usually a sign of significant heart disease.

 Definitive treatment is transvenous pacing, but as a temporary measure, the
ventricular rate can be improved with an infusion of isoprenaline.

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 Sustained, severe HTN is associated with MI & CVA
 Need to treat underlying cause before any antihypertensive medication is given

 DBP > 110 definitely abnormal
 Sustained hypertension needs to be treated


 Pain: NEVER give antihypertensives to a patient in pain
 Anxiety
 Drugs: inotropes
 Hypercapnea/hypoxia
 Full bladders (especially in elderly, confused people)
 Malignant hyperthermia
 Hormonal: pheochromocytoma, thyroid crisis, carcinoid …

 Undiagnosed hypertension. Brought out by surgery
 Hypertension inadequately controlled before surgery
 Patient mistakenly advised not to take regular medication preop

 Oxygen
 Goal is short-term control

Nifedipine SL
 Sublingual nifedipine 10mg.
 Can be written PRN - 10 mg SL up to q2hr for systolic BP > 170

Labetalol IV
 For those who cannot take sublingual medication because of sedation, poor
cognitive function on non-cooperation (consider pain or full bladder) or for
those in which nifedipine is ineffective.

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 Titrate IV dose against effect, giving 5mgto start with. After 5-10 min if no
effect, give 10mg, then 15 mg etc.
 Contraindicated in asthma and cardiac failure.

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Myocardial Ischemia
 MI is the single biggest killer in the perioperative period.
 pOP MI often does not generate the typical signs & symptoms. Chest pain may
be masked by analgesic/anesthetic medication.
 pOP MI occurs most frequently 48-72 hr after surgery
 Needs careful monitoring just like for DVT: identify patients at risk and employ
full range of simple measures to prevent ischemic complications.

Patients at risk
 Previous MI (especially within last 6 months) or known angina
 Hypertensives (especially those with EKG evidence of LVH)
 Diabetics
 The elderly
 Vascular surgery patients (concomitant CAD)
 Smokers
 Those with EKG evidence of “strain,” bundle branch block or old MI

 Avoid anything that upsets the balance of myocardial oxygen supply and demand.
Avoid tachycardia, hypotension, hypertension and hypoxia.

Fluid Balance
 Ensure good hydration/adequate UO. Avoid anemia (Hb > 10 mg/dl)

 Pain is very bad for the heart

 Patients will have hypoxia for 3 or 4 days pOP, particularly at night. Prescribe
oxygen for at-risk patients

 Treat accordingly

Regular medication
 Continue all cardiovascular medications. Remember that NTG can be given as a
transdermal patch.

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 The more the better. Pulse oximeter or automatic BP if feasible

DVT prophylaxis
 SQ heparin & TEDs

 Examine for evidence of hypotension, CHF or dysrhythmia
 Treat CP with increments of IV MS
 Employ preventative measures above
 Bed rest
 Get 12-lead EKG & compare to preop EKG
 Send blood for serial CKs. CK levels are normally elevated pOP so be sure to
ask for isoenzymes
 Consult medicine/cardiology.

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Pulmonary Edema
 Pulmonary edema is an abnormal accumulation of fluid in the extravascular
spaces and tissues of the lung.
 It is not an uncommon cause of respiratory distress in surgical patients.


Starling forces
 Starling forces describe the flow of fluid in an out of the pulmonary capillary.

35 20 5 20

Arterial Venous

 Most of the fluid forced out at the arterial end passes back into the capillary at
the venous end; the rest drains out via the lymphatics.
 If excessive fluid leaks from the capillary, pulmonary edema results.

Interstitial Edema
 Characterized by engorgement of the interstitial space.
 Effects on lung function are subtle; the lungs become stiffer and the patient
usually complains of SOB.
 Some radiological changes

Alveolar Edema
 When fluid passes into the alveoli themselves.
 Dramatic clinical effects with shrinking of the alveoli, stiffer lungs, increased
work of breathing and impaired gas exchange.
 The transition from interstitial to alveolar edema tends to occur suddenly.

 Increased hydrostatic pressure in the capillary (e.g. LV failure)
 Reduced colloid pressure (e.g. hypoproteinemia)
 Increased capillary permeability (e.g. in aspiration pneumonitis or ARDS)

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Cardiogenic pulmonary edema

 The diagnosis should be obvious clinically

 PMH: Like to occur in a patient with known ischemic, hypertensive or
rheumatic heart disease
 Associated with over-enthusiastic fluid therapy
 Sx: Patient complains of sudden, severe dyspnea made worse by lying

 Gen: sweating, cool peripheries, sputum is pink/frothy
 VS: tachycardia, tachypnea, hypertension. Hypotension is a grave sign
indicative of cardiogenic shock.
 Chest: B/L basilar rales; there may be an audible wheeze
 CV:raised JVP, gallop rhythm with an S3. Murmurs may be present and a new
murmur is a significant finding.

 CXR: A normal-sized heart strongly suggests a non-cardiogenic
 EKG: looking for AMI or dysrhythmia
 Cardiac enzymes: for r/o MI. If the patient has had recent surgery, be sure to
ask for CK-MB (isoenzymes).
 Echo To study valve function, myocardial contractility and EF.
 CVP not necessary for diagnosis in the acute case.
 ABG When respiratory failure is suspected.

“Borderline cardiac failure”

 Patients with chronic heart disease while not in overt failure are at risk of
developing pulmonary edema. Factors which may tip the balance:

Fluid overload
 Patients with chronic heart failure cannot cope with a wide range of filling
 However, fear of this complication leads to a tendency to be excessively miserly
with IVF

Systemic vasoconstriction
 Causes a redistribution of fluid from the systemic to the pulmonary circulations
as with pain, hypothermia or the wearing-off of anesthetic drugs.

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Myocardial ischemia/infarction or dysrhythmias


Initial management
 Sit up, give adequate oxygen by face mask
 If there is evidence of cardiogenic shock or oliguria get help early
 Titrate in some IV narcotic (MS 2mg at 2 min intervals up to a maximum of 10
mg). This reduces venous tone and alleviates agitation and anxiety
 Furosemide / Lasix (20 - 40 mg IVP). The immediate effect of this drug is
venodilation which reduces preload. Later there is a diuresis.
 Proceed to advanced management (with medical/ICU consultation) in severe or
refractory cases.

Advanced management
 Identify and treat dysrhythmias
 Consider vasodilators (e.g. isosorbide dinitrate IV)
 In severe cases intubate and start mechanical ventilation
 Further measures are required for cardiogenic shock (hypotension, oliguria) or
respiratory failure. These include inotropes, invasive monitoring, ventilation, and
one-to-one nursing … ICU

Non-cardiogenic pulmonary edema

 ARDS Final common pathway for a variety of major insults such as trauma,
shock, sepsis, pancreatitis, burns, obstetric disasters or MSOF. The basic
mechanism is an increase in capillary permeability.
 Pulmonary aspiration of gastric contents
 Pneumonias and sepsis
 Allergic reactions to drugs or blood products
 Neurogenic pulmonary edema. A rare condition in which pulmonary edema
accompanies an acute intracranial lesion such as head injury, tumor, or

 Suggested by an absence of specific features of cardiac failure.
 Usually obvious from the history alone.
 The diagnosis can be confirmed by pulmonary edema in the presence of a
normal-sized heart, or normal PCWP.

 Specific treatment depends on the precipitating cause

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 Supportive management includes ventilation, optimization of filling pressures and

maintenance of colloid oncotic pressure by avoidance of hypoproteinemia.

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Cardiac Arrest
Who to resuscitate?
 DNR is appropriate when CPR is unlikely to succeed, where it is contrary to the
expressed wishes of a competent patient, or where CPR is likely to be followed
by a length or quality of life which is unacceptable to the patient. DNR on the
basis of age alone is not appropriate.
 The decision for DNR rests ultimately with the responsible attending. The
decision should be taken as soon as possible where arrest is deemed likely. The
decision should be reviewed regularly.
 When a DNR order is taken, it should be documented clearly in the chart, and a
brief rationale given.

DNR vs. Withdrawal of treatment

 It may be appropriate to continue various supportive measures in a patient who is
the subject of a DNR order.
 Treatment aimed at alleviating suffering should always be continued.

Basic life support

Call for help

 Look for verbal response.
 Open and maintain the airway with jaw thrust/chin lift and head extension

 Listen at the lips while watching the chest.
 If there is no apparent respiratory effort begin mask resuscitation.

 Feel for a carotid pulse (for 5 sec). If absent, start external cardiac massage at a
rate of 80/min.
 Place one hand on top of the other, on the lower sternum, and give sharp
compressions to depress the sternum by 3-4 cm each time. If alone give 15
compressions for every two breaths.

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Advanced cardiac life support

General measures
 Intubation, mask ventilation or mechanical ventilation, and securing of IV access
should be performed.
 An EKG monitor should be connected.
 For witnessed arrests, a pre-cordial thump is recommended.
 Further treatment then depends on the heart rhythm

VF or pulseless VT
 DC shock 200J, 200J, 360 J
 Epinephrine 1mg IV
 Continue CPR
 Shock 360, 360, 360
 Consider lidocaine 100 mg (= 5 ml of 2%) or bretylium

Asystole (where VF cannot be excluded)

 Shock 200, 200, 360 then as for asystole

 Epinephrine 1mg IV
 Continue CPR
 Atropine 3 mg IV qD
 Consider pacing

Electromechanical Dissociation
 Differential diagnosis is hypovolemia, tension pneumothorax, pulmonary
embolism or cardiac tamponade. Consider specific therapy for each.
 Epinephrine 1mg IV
 Repeat as required.

When to give up

If cardiac output restored

 If cardiac output is restored admit to ICU for further management.
 Prognosis depends on the underlying cause of the arrest and the hypoxic interval;
the longer the hypoxic interval the greater the chance of neurological damage.
 Arterial pH correlates well with outcome. If pH > 7.20, the outlook is
reasonable. Survival where the post-arrest pH < 7.0 is poor.

If cardiac output not restored

 Decision has to be made on when to discontinue CPR. Normally, 20 minutes of
unsuccessful resuscitation is considered enough.

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Indications for prolonged resuscitation include:

 Hypothermia CPR should be continued until body temperature is normal.
Rewarming may require cardiopulmonary bypass.
 Suspected drug overdose
 Any arrest in children who tend to have a better neurological prognosis than
 During prolonged resuscitation, epinephrine 1 mg IV is given every 5 minutes.
Bicarbonate should only be given for severe acidosis (pH < 7.0) as documented
on blood gas analysis.

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Respiratory Problems
Effects of surgery and anesthesia on respiratory function
 There are four major effects, decreased lung compliance, ventilation/perfusion
mismatch, hypoventilation and ciliary dysfunction.

1. Decreased lung compliance

 Stiffer lungs

2. Ventilation/perfusion mismatch
 Anesthesia and surgery upset the delicate mechanisms that usually match
perfusion to ventilation

3. Hypoventilation

Central causes
 Respiratory depressant effects of anesthetic agents, opioids or CNS pathology

Peripheral causes
 Obesity
 Abdominal distention
 Tight dressings
 Pain
 Any lung pathology which increases the work of breathing (e.g. bronchospasm or
sputum retention)

4. Ciliary dysfunction
 Giving dry gas directly to the airway has a damaging effect on respiratory mucosa
and ciliary function.

Overall effects
 Common finding after surgery is hypoxemia (worse in the presence of chronic
lung disease.
 Dips of oxygen saturation to < 50% are commonplace after major abdominal
surgery. Episodic hypoxemia occurs especially at night, within 72 hours of the
operation. It is known that this hypoxia is associated with episodes of severe
myocardial infarction.

Preventative measures
 Identify patients at risk: abdominal or thoracic surgery, elderly, smokers,

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 Prescribe oxygen therapy.

 Ensure good analgesia

Oxygen therapy


Standard facemask
 Cannot deliver very high concentrations of oxygen.
 The exact FIO2 depends on the pattern of breathing.
 High respiratory rates will be closer to RA while deeper breathes will have higher
oxygen concentrations.

High-flow masks
 Jet of oxygen is passed through the mask.
 Come in a selection of concentrations 28%, 28%, 35%.
 Are the preferred mode of delivery for patients with significant chronic lung
 The highest concentration is 35%.

Non-rebreather masks
 The reservoir bag fills up with oxygen during expiration.
 Can deliver up to 85% oxygen.

Nasal cannulae
 Used for comfort
 Cannot give high concentrations of oxygen and are thus not suitable for very sick


Respiratory depression
 A small subset of patients with chronic lung disease have grossly abnormal blood
gases. As a result of long-standing lung damage, they have chronically increased
work of breathing and by consequence such hypoventilation that their central
chemoreceptors are extremely tolerant of very high levels of CO2.
 Their kidneys compensate for the respiratory acidosis by retaining bicarbonate, so
the arterial pH is near normal.
 Instead these patients rely on hypoxia for respiratory drive.
 Giving oxygen will depress the respiratory drive further increasing the CO2
resulting in depression of consciousness and apnea. If the oxygen is
discontinued, hypoxia will return but the CO2 levels will be too high to be
overcome and unless the patient receives mechanical ventilation he will die.
 Hypoxic drive is rare
 Controlled oxygen delivery is the key … do not use face masks but rather use
high-flow oxygen delivery which can be titrated.

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Identifying patients with hypoxic drive

 Patients are bright blue
 History: long h/o of COPD. Shortness of breath at rest or minimal
exertion. Bronchospasm, chronic purulent cough. Previous uneventful general
anesthesia makes hypoxic drive extremely unlikely.
 Exam: Cyanosis and asterixis (flapping tremor)
 Labs: Blood gases (low PaO2 (< 75 mmHg) and high PaCO2 (> 55 mm
Hg) and slightly low or normal pH under RA. Be suspicious if bicarbonate is >
30 mmol/l.

Controlled oxygen therapy

 Giving progressively increased concentrations of oxygen and at each step
measuring blood gases after 10 minutes or so.
 If you see an increase in PaO2 without an increase in PaCO2 it is safe to proceed
to the next concentration up.
 If you see an increase in PaCO2, go back down to the step before and prescribe
this much oxygen.

Oxygen toxicity
 Said to occur if concentrations of > 60% are inhaled for long periods (i.e. > 24
 Hypoxia should never be tolerated because of fear of oxygen toxicity.

Retrolental fibroplasia
 See in neonates who are ventilated with high oxygen concentrations, causing
fibrosis behind the lens of the eye, and blindness.

 See with inveterate, chronic smokers who can’t resist one last drag while on
oxygen therapy.

 Cyanosis or documented hypoxemia (as with a pulse oximeter)
 Major surgery (24 h postoperatively and at night for 3 nights)
 Shock and severe hemorrhage. Any cause of shock results in a reduction of
oxygen delivery.
 Myocardial ischemia or those at risk of it.
 Conditions of high metabolic rate. For example, fever, rigors, thyroid crisis,
malignant hyperthermia.
 Reduced consciousness or hypoventilation

Analgesia and respiratory dysfunction

 Any source of pain which prevents movement, deep breathing or coughing will
hamper a patient’s ability to clear secretions from the lungs.
 The resultant immobility and sputum retention is a potent recipe for pneumonia.

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 However, excessive, or ill-chosen analgesic regimens can also have an equally

catastrophic effect.
 All opioids have respiratory-depressive properties which is especially dangerous
in decompensated patients.

Epidural analgesia
 The gold standard.
 Provides the most effective pain relief available allowing movement and coughing
without pain.
 The respiratory side-effects are comparatively trivial.

IV opioids
 Need to titrate.
 Therefore the best is PCA.
 For patients with airway disease fentanyl is preferred over morphine because it
causes less bronchospasm.

Opioids by other routes

 Intermittent injection should be avoided.
 All opioids have respiratory depressive effects. So-called “weak opioids” also
cause respiratory depression in proportion to their analgesic effects.

Peripheral nerve blocks

 Excellent for surgery in the peripheries.
 Avoids opioids

 Are an effective adjunct to postoperative pain management and reduce the
requirement for opioids.
 Significant incidence of bronchospasm; the effect is often delayed.

Sputum control
 Humidified oxygen
 Good general hydration.
 Pain relief
 Chest PT: including percussion and postural drainage.

Respiratory distress
 Differential diagnosis
 Asthma
 Pneumonia, collapse, consolidation
 Pulmonary edema
 Pulmonary embolus
 Pneumothorax

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 Pulmonary aspiration
 Pleural effusions

Asthma and bronchospasm

 Worsening asthma is heralded by dyspnea, audible wheeze and the use of
accessory muscles.

Five important danger signs;

1. Tachycardia > 120 (although most often caused by treatment
with -2 agonists or theophylline). Bradycardia in acute asthma
is an indication for a code.
2. Inability to speak
3. Silent chest (signifies severe hypoventilation)
4. Cyanosis or SaO2< 93%
5. Depressed consciousness

 CXR to exclude pneumothorax, pneumonia or aspiration
 ABGs (a PaCO2 in the normal range is bad, suggesting impending deterioration).
Patients with acute asthma who are coping well usually hyper ventilate with a
PaCO2 or 25-30mmHg

 Humidified oxygen
 salbutamol / and iptraropium / Atrovent by nebulizer
 IV steroids (hydrocortisone 200 mg q6hr for average adult)
 The quantity of nebulized bronchodilator that reaches the lower airways in acute
asthma is small, and if a single nebulizer has limited effect, it should be
immediately followed by another, then another. Each nebulizer then becomes
more progressively more effective. Four-hourly nebulizers are for maintenance,
not emergency management.
 Sedatives are absolutely contraindicated. Opioids should also be avoided if at all
possible. Consult pain service/anesthesia if severe pain coexists.

Pneumonia, collapse and consolidation

 Nosocomial pneumonia occurs in 0.5 - 5% of all in-patients and 10 - 40 % in the
 Commonest causative organism is Strep. Pneumoniae but Gram-negative organisms
are seen more often than in community-acquired pneumonias.
 Diagnosis, suggested by cough, fever, purulent sputum and consolidation on
CXR should be confirmed by blood cultures.
 Sputum clearance is even more important than antibiotics. Involve chest PT

Pulmonary edema
 Pulmonary edema is a potent cause of respiratory distress, hypoxemia and
ventilatory failure.

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Pulmonary embolus
 Any patient laid up in bed after surgery is at risk.
 Of PEs, 40-60% are asymptomatic; 10% are fatal. The common signs are non-
specific, and the specific signs are rare, though pulmonary embolus should always
feature in the differential diagnosis of respiratory distress.
 PE is a diagnosis of exclusion.

 Dyspnea: common. Sudden onset of SOB is the most reliable indicator.
 Syncope: occasionally
 Pleuritic chest pain and hemoptysis: this occurs in pulmonary infarction, which is
only rarely a consequence of PE.
 Palpitations: AF can occur if there is pre-existing cardiac disease.

 Tachycardia and tachypnea: common
 Low-grade fever: may occur
 Wheeze: sometimes
 Hypotension common in massive PE.

 CXR minimal change. There may be some loss of volume. Infarction
(with the classic ‘wedge’ appearance) and pleural effusion is rare.
 EKG Sinus tachycardia is the usual finding. Acute-onset AF may be seen.
S1Q3T3, right axis deviation and RV ischemia are rare.
 ABG may show reduced PaO2 but not always. PaCO2 is usually low.
 Scans Perfusion scan can exclude; V/Q scan required for definitive proof
of diagnosis.

 Most patients with a PE will be dyspneic, tachycardic with a normal CXR and
sinus tachycardia on the EKG with no other signs.
 Need to decide whether to heparinize.
 Exclude other causes: pulmonary edema, pneumothorax, pulmonary collapse,
consolidation, aspiration.
 If there are no other likely causes, then a PE can be presumed and a request for a
V/Q scan made at the earliest opportunity.

 Make sure there are no contraindications to anticoagulation
 If not, then give 5000 U IV followed by an infusion of 20,000 - 24000 U per day.
 Monitor the clotting times regularly. A PTT of 2-3 times control is required. If
clotting times fall below this, it is usually necessary to give a bolus (e.g. 2000
Units) as well as increasing the infusion rate.
 If the diagnosis is confirmed with a scan, treatment with warfarin will be required
for 3-6 months.
 Remember interactions with aspirin

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 May be spontaneous, trauma-related or iatrogenic

 Occur in tall, thin males, or in those with
 COPD/asthma

 Rib fractures, or
 penetrating chest wounds

 Central line insertion
 Brachial plexus block
 as a result of some forms of surgery (e.g. nephrectomy)

 Index of suspicion with a dyspneic patient
 Upright CXR

 Large PTX managed with chest tube drainage
 Small non-traumatic ones can sometimes be managed by aspiration or watched
with serial chest x-rays.

Pulmonary aspiration
 Results from inhalation of gastric contents

Predisposing factors
 anesthesia
 emergency surgery
 depressed consciousness
 disorders of swallowing or cough
 use of NG tubes
 pregnancy and tracheostomy

 Dyspnea
 Wheezing
 Cough
 Rhonchi
 CXR changes include multilobar infiltrates which may be alveolar or interstitial
and may be unilateral

 Supportive including humidified oxygen, hydration and artificial ventilation.

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 Antibiotics are indicated only if there is definite evidence for infection, and are
usually aimed at Gram-negative organisms.

Pleural effusions
 An effusion seen on a CXR is at least 150 ml
 An effusion picked up clinically is likely to be huge.
 Needle drainage is indicated where respiratory function is borderline

The emergency CXR

Collapse (atelectasis)
 Increased opacity of the affected lobe
 Loss of volume where the three main changes seen are:
1. Raised hemidiaphragm
2. shift of mediastinal structures towards the lesion,
3. crowding of ribs on the affected side
 Hyperlucency of adjacent unaffected lobes is sometimes seen, as they
hyperexpand to help fill the space left by the collapse.

 Ill-defined margins
 Irregular shape
 no loss of volume (no mediastinal shift, raised hemidiaphragm, no rib crowding)
 air bronchograms are common

 Classical picture of community-acquired “lobar” pneumonia (Strep. pneumoniae) is
uniform consolidation in a single lobe with air bronchograms and no loss of
 Nosocomial pneumonias (gram-negative bacteria or Staph. aureus) may show
patchy segmental consolidation which may be bilateral and predominately affect
the lower lobes. Air bronchograms are rarely seen and there may be loss of

 Two findings which are required for the diagnosis of pneumothorax:
1. loss of vascular markings at the apex, and
2. laterally a visible lung edge
 On a supine film the air collects anteriorly, which is more difficult to spot, but
clues are a unilaterally lucent lung, or a translucent band parallel to the
mediastinum or diaphragm.
 A tension pneumothorax is seen when mediastinal structures are displaced to
the opposite side.
 Tension pneumothorax is, however, a clinical diagnosis, which must be treated

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Pleural effusion
 A large pleural effusion (300 - 500 ml) should be easy to detect on an erect chest
 Signs are a homogenous opacification of the lower chest, with loss of
costophrenic angle and hemidiaphragm. The upper margin is concave upwards
and higher laterally than medially.
 The signs of a small pleural effusion are usually loss of the costophrenic angle.

Pulmonary edema
 An excess of fluid in the lungs that is not in the intravascular compartment.
 Initially the fluid is in the interstitial spaces and, as it worsens, it eventually spills
into the alveolar air spaces.

Interstitial edema
 Septal lines: fluid collects in the interlobular septa which is visible as short,
horizontal lines 3-6 cm long, known as Kerley ‘B’ lines. They are best seen in the
peripheral lower zones.
 Peribronchial cuffing: On normal x-rays a few bronchi can be seen end-on in
the hilar regions. In interstitial edema their walls appear thickened.
 Vascular changes: Vessel shadows are seen more clearly in the upper zones
than lower, referred to as cephalization.

Alveolar edema
 Irregular shadowing: Gray fluffy shadows are seen, more frequently in the
lower zones. As it progresses, the shadows become confluent and whiter.
Sometimes the hilar zones are more affected give a “bat’s wins” appearance.
 Pleural effusions: commonly bilateral, but if unilateral more common on the
right. Fluid may be seen in the horizontal fissure.
 Air bronchograms: common.

Respiratory failure and ventilation

 The lung has two functions: taking up oxygen and getting rid of carbon dioxide
 The vast majority of cases, the respiratory failure results from both poor
oxygenation and hypoventilation.
 Treatment is intermittent positive pressure ventilation (IPPV).
 Provide adequate ventilation to control PaCO2 and thus removes all work of
 Less work of breathing also decreases oxygen demand.
 High oxygen concentrations can be delivered and PEEP applied which improves
 PEEP increases the functional residual capacity (FRC) and reduces shunt (blood
passing through unventilated areas of lung).

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Oliguria & Catheters

 Low UO is an important sign of hypovolemia and may precede ARF. Aim for a
UO of at least 0.5 ml/kg/hr (1.0 ml/kg/hr in children). The minimum excretion
of sodium load requires a volume greater than 20ml/hr.

 Catheterize all high-risk patients: diabetics, CRF, Jaundice, Elderly, CHF, severe
CT Dz.
 Catheterize all major surgeries: major trauma/crush injuries,
burns/electrocutions, hypovolemia/hypoxia, sepsis, major
abdominal/vascular/cardiac cases.
 Exam: (pulse, BP, mental status, skin turgor, eye turgor, dry mouth).
 Always consider the possibility of urinary retention/obstruction & examine for
full bladder. Retention is a common cause of postop confusion.
 Exclude signs of heart failure or fluid overload
 Consider furosemide / Lasix dependence

Management of Oliguria

Role of Fluids
 Correct the fluid deficit (with 250 cc of fluid challenge) -> then reassess.
 If no initial improvement then repeat the challenge; consider placing CL -> CVP

Role of Diuretics
 Diuretics can only be used when there is accurate knowledge of volume status
 Consider furosemide dependence

Role of Inotropes
 Consider dopamine (2.5 mcg/kg/min) if volume status is normalized & UO still

General care
 Oxygen
 Check for any nephrotoxic drugs (aminoglycosides, NSAIDs, diuretics).

Diagnosis of ARF
 Kidney has lost ability to concentrate urine

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ARF Hypovolemia
Dilute urine Concentrated urine, low volume
Iso-osmotic with plasma specific gravity > 1.016
High sodium content Low sodium content (< 20 meq/l)
Low urine/plasma urea ratio High urine/plasma urea ratio
Low urine urea content High urine urea content

 Indications
1. accurate measurement of UO
2. management of urinary retention
3. compromised micturition
4. bladder irrigation

Urethral catheters
 Use a urojet for analgesia/lubrication; takes time to work
 Antisepsis
 Take weight off bladder neck by taping to leg
 Clamp catheter distal to insertion of inflation channel
 Replace foreskin after catheterizing males

Suprapubic catheterization
 Preferred for management of acute retention
 Contraindications: no distended bladder, post-TURP, in patients with bladder

Catheter problems

 Unblock with a bladder syringe & NS
 Bladder washout
 If unsuccessful, may need to change catheter

Leaking around the catheter

 From blockage of lumen but mostly from detrusor instability
 Change the catheter for a size smaller

Acute retention
 Common after major surgery, particularly in males .... associated with prostatic
 Increased with epidural analgesia

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 Catheterize for painful retention only ... exception is with epidural analgesia
where pain may be masked.

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Normal postoperative fever

 Stress of surgery may cause a low-grade fever of 37 to 37.5. It is therefore not
usually necessary to work-up every fever in the early postoperative period.

Non-septic causes
 DVT, Blood transfusion reactions, malignant hyperthermia, drug reactions

Septic causes

 Anesthesia + surgery impair sputum clearance. Common pathogen is still Strep.

 Staph. aureus, Gram-negative bacilli like E. coli & anaerobes.

 Especially after urine catheterization/instrumentation. Gram-negatives such as
E. coli.

 In any patient with a central line … especially > 1 week.

 After neurosurgery - especially VP shunt

 Ischemic limbs can get infected with anaerobes. Orthopedic implants can get


 W/U only necessary for temperature > 38. Check oral, rectal or tympanic
measurements. Oscillating fevers are suggestive of an abscess..

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 Check recent microbiological history. Note special problems such as

immunocompromise, burns, splenectomy …

 Check for other signs of sepsis: tachycardia, tachypnea, warm extremities, wide
pulse pressure, rigors, hypotension
 Check clues as to focus: cough/sputum, dysuria, cloudy urine, purulent wound
drainage, peritoneal signs, meningism, long-standing central line.

 Check WBC, C-reactive protein, CXR

 Key to good microbiological practice.
 Take appropriate specimens before starting empirical antibiotic therapy.

Blood cultures
 Blood cultures. Chance of catching bacteremia is about 60 - 70% with a 10ml
sample. False positive (contaminants) are common.
 Technique: prep a wide area of skin. Let alcohol dry first. Take 10 ml of blood,
then discard needle. Place 5 ml in each bottle using a fresh needle.
 The best time to take blood cultures is just before the peak of temperature.

 Mid-stream urine specimen is useful.
 Finding of significant WBC indicates UTI
 Catheter specimen less useful as WBC may be a normal finding

 Sputum is always full of normal flora.
 The only truly significant result is a heavy growth of a known respiratory
 Blood cultures are a much more productive way to investigate suspected

 Collected by LP
 Send for gram stain/.microscopy immediately

Wound swabs
 Get frank pus
 Wipes of erythematous areas not useful

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Non-antibiotic treatment
 Sputum clearance: good analgesia & PT
 For wounds remove one or more sutures. All abscesses require surgical
exploration and drainage.
 For UTI remove catheter. Increase UO. Alkalinization of urine helps alleviate
 DC CL; send tip for Cx

Antibiotic treatment
 Take cultures first

 First choice is cefuroxime 1.5 g IV q8. Useful coverage for Staph. aureus, E. coli
and Gram-negatives and Strep. pneumoniae.
 If you suspect anaerobes (after GI/abdominal surgery) add metronidazole /
Flagyl 500mgIV
 If patient received cefuroxime perioperatively then try amoxicillin + clavulonate /

Complicated -> get ID consult

 Recent course of Abx (other than prophylaxis)
 Immunosuppression / neutropenia
 Serious illness, septic shock, burns, MSOF
 Failure of treatment
 known allergy to first-line agents
 known resistant organism (MRSA, VRE)
 Unusual focus of infection

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 Mild 35 -37; Moderate 32 - 35; Severe < 32

 Anesthesia -> decreased BMR
 Temperature regulation altered
 Normal responses to hypothermia inhibited
 Loss of evaporative heat during surgery
 Use of unwarmed IVF.

Patients at risk
 Extremes of age
 Thoracic/abdominal surgery
 Prolonged surgery
 Emergency surgery
 Massive blood transfusion
 Hypothyroidism or malnutrition


 Vasoconstriction/shivering -> increased myocardial oxygen demand
 Severe hypothermia -> dysrhythmias and VF
 Increased blood viscosity

 Shivering increases oxygen consumption -> hypoxemia
 Give oxygen to shivering patients
 Oxy hemoglobin curve stabilized

 Progressive depressed LOC
 Fixed & dilated below 28

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 Decreased clotting function
 Renal/hepatic function decreased
 Hyperglycemia secondary to decreased glucose utilization

Technical problems
 BP measurement difficult; automatic machines misread
 Pulse oximeters may fail due to poor peripheral perfusion
 Phlebotomy difficult

Measurement of body temperature

 Never take axillary temperature
 Oral (rectal more reliable)
 Infrared tympanic membrane thermometer
 Nasopharyngeal/esophageal probes ... reliable for use in unconscious/ventilated

 Oxygen
 Passive rewarming (remember to cover the scalp)
 Active surface rewarming ... may cause vasodilatation -> hypotension; treat with
 Active core rewarming (cardiopulmonary bypass or ECMO)

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CNS complications
Confusion: Definition

 Used to describe a syndrome of acute, fluctuating disturbance of attention,
memory, sleep, orientation, perception and psychomotor function.
 Usually occurs in the first few days post-op, often after a lucid interval.
 It is typically worse at night.
 Not all patients will be agitated (some will be withdrawn)

 Differs from delirium in having a gradual onset and in being largely irreversible.
 It also shows as a global cerebral impairment.

 May co-exist or mimic delirium and/or dementia.
 Many of the symptoms overlap and may confuse the diagnosis.

Confusion: Definition

Quick MSE
 Check with a set of simple test for memory and orientation.
 Ask for patients age, the time, the date, the name of the hospital and the
 Ask about the date of a major historical event.
 Ask them to identify staff members by their uniforms
 Ask them to remember an address and repeat it back to you.
 Ask them to count backwards from 20.

Delirium vs. Dementia

 Delirium is an acute condition; dementia is chronic.
 The family can be very useful in comparing pre- vs. Post-operative states.
 Remember that: dementia can appear to be worse in unfamiliar surroundings and
that demented patients can suffer delirium.

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Causes of delirium

 Hypoglycemia, hyperglycemia, dehydration, hyponatremia, uremia, acidosis,
hypophosphatemia, hypercalcemia, hypocalcemia, hypothyroidism,
hyperthyroidism, hepatic failure, porphyria.

 Hypoxia, infection, pulmonary embolus, fat embolus.

 Respiratory, urinary, wounds, intra-abdominal.

 Myocardial infarct, congestive heart failure, hypotension.

 Raised ICP, brain contusion, reduced perfusion, post-ictal state, CVA/TIA, post-
cardiac bypass, infection, sensory/sleep deprivation.

 urinary retention, constipation

 iatrogenic or withdrawal

Review drug chart

 Analgesics opioids
 Local anesthetics in overdose
 Psychotropics benzodiazepines, tricyclics, haloperidol / haldol.
 Anti-emetics prochlorperazine / Compazine, metoclopramide / Reglan,
 Anticholinergics atropine, hyoscine.
 Steroids

 In all cases, hypoxia, electrolyte imbalance, myocardial ischemia and infection
needs to be actively excluded.
 CBC anemia, leukocytosis (2o to infection)
 Lytes, BUN, Cr Dehydration and electrolyte imbalance
 Glucose hypo/hyperglycemia
 Urinalysis both for microbiology & chemistry
 Gases ± oximetry for hypoxia or acidosis.
 EKG ± enzymes for ischemia, infarct or dysrhythmias
 Radiology CXR, U/S, CT scans, V/Q scans
 Biochemistry thyroid function, drug screening, porphyrins.

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Management of Delirium
 Treatment takes two forms:
1. Dealing with the cause of the delirium
2. Supportive care to prevent deterioration or injury

Nursing care
 Implement measures to minimize risk of injury.
 Less experienced nurses may be inclined to rely too much on sedation and
should be politely resisted until you are sure that it is indicated.
 Restraints are very rarely a good idea; they worsen the agitation and increase the
risks of injury.

 Dehydration causes delirium and delirium causes dehydration.
 Good fluid and electrolyte control is essential and is likely to need secure IV
access, repeated investigations and measurement of urine output.
 This can be difficult with an uncooperative patient.

 Hypoxia is common, especially at night.
 All patients who have had major surgery should receive oxygen at night.
 All delirious patients should have at least a trial of oxygen, along with serial gases
or oximetry to find if they are helped by it.
 Persistent hypoxia with delirium despite oxygen is likely to mean a transfer to the

Nutrition & vitamins

 Adequate calories and protein intake needs to be continued; often by the
nasogastric route.
 Vitamin B-12 may be indicated if there is good evidence of alcoholism or
chronic deficiency.

 Should be a last resort, not an automatic reaction to delirium.
 Most sedatives can cause delirium and that many are respiratory depressants.
 When sedation is essential it is best given in regular small doses.
 Benzodiazepines are respiratory depressants, long-acting and disturb normal
cognitive function; unless they are specifically indicated they should be avoided.
 Haloperidol /haldol is a good choice and can be given orally in doses of 0.5 -
2.0 mg q6hrs.
 Thioridazine / Mellaril is an alternative in doses of 5 - 10 mg q 8hr. This dose
can be increased to a maximum of 30 mg q8hrs.

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 Rule-out pain, delirium, withdrawal or depression.

 Essential to pick a short-acting agent to avoid daytime sedation.
 Try Serax 10-15mg PO.
 Problems include respiratory depression and addiction.
 All patients must be warned that hypnotics are extremely habit-forming and
should be used infrequently, irregularly and only in the short-term.
 Reduce the dose in the elderly and avoid benzodiazepines altogether when
respiratory function is critical.

Other sedative drugs

 Tricyclic antidepressants have sedative properties and improve sleep in depressed
 Antihistamines
 Opioid analgesics are powerful respiratory depressants and should only be used
in the ICU.

 Coma is never a normal finding, nor is it safe to attribute it to anesthesia.
 When there is good reason to suspect drug-induced coma a therapeutic trial of a
specific antagonist is reasonable.
 Naloxone / Narcan (0.1 to 0.2 mg) reverses opioid sedation but also the
analgesia.; short duration of action and may require several doses.
 Flumazenil / Romazicon (200 mcg IV) reverses the effects of benzodiazepines.
 If coma persists think about ICU.

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 Brain contusion, infections, raised ICP, epilepsy, CVA

 many agents in overdose including lithium, tricyclics, aminophylline, NSAIDs,
anti-emetics, local anesthetics

 commonly alcohol

 hyponatremia, hypoglycemia, hypercalcemia, hypomagnesemia

 hypoxia, alkalosis

 febrile convulsions in children

 eclampsia


 Maintain a clear airway
 Supplemental oxygen
 Prevention of injury

 Emergency drug of choice is diazepam / Valium (10 - 29 mg IV slowly or 10 - 20
mg PR). This can be followed by phenytoin / Dilantin (15 mg/kg IV slowly).
 Continued seizures may require general anesthesia.
 The cause of the fit must be vigorously pursued with clinical and laboratory tests.
Don’t forget a pregnancy test in young women.

Extrapyramidal problems
 Pre-existing Parkinsonism may worsen during a surgical admission due to
difficulty in administering the medications.

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 Extrapyramidal symptoms such as rigidity, tremor, dystonia, akathisia, tardive

dyskinesia and oculogyric crisis may be precipitated by many drugs used
 Notably anti-emetics (droperidol, metoclopramide / Reglan, prochlorperazine /
Compazine) and antipsychotics (chlorpromazine / Thorazine and haloperidol /
 These should be used with caution in the elderly and avoided whenever possible
in Parkinsonian patients.
 Antimuscarinics (benztropine mesylate / Cogentin) 1-2 mg PO/IM qD/bid are
used to treat symptoms of drug-induced Parkinsonism.

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 Thrombosis is a common consequence of anesthesia and surgery. Occurs in up
to 25% of all surgical procedures.
 Arises from:
1. Abnormal blood flow,
2. Hypercoagulability,
3. Endothelial injury.

High-risk groups
 Orthopedic surgery
 Gynecological surgery
 Cardiac failure
 Malignancy
 Obesity
 Elderly, strokes & generalized immobility
 Progesterone/Estrogen therapy
 PVD/varicose veins
 h/o DVT/PE
 Unusual hypercoagulable states

 Early mobilization (with adequate pain control).
 SQ heparin (5000 U SC x 5 days) -> thrombocytopenia occurs in 0.3%.
 TEDs (TEDs + heparin may be additive).
 Pneumoboots.
 Epidural/spinal anesthesia.
 Coumadin (especially for orthopedic surgery).


 DVT is commonly asymptomatic.
 Calf pain (redness, swelling and engorged superficial veins). Positive Homan’s
 Groin pain (with iliofemoral thrombosis).
 Cyanotic discoloration of affected limb.

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 Calf DVT -> PE rare.
 However, calf DVTs may extend proximally.
 Treat with heparin ... then continue anticoagulation for 3 months.

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Miscellaneous Postoperative
Thyroidectomy problems

Airway obstruction

Postoperative hematoma
 May be dramatic.
 Management is to remove the skin closure clips and evacuate the clot at the bedside.

Laryngeal edema
 Sometimes occurs on the 2nd or 3rd day and is gradual in onset.
 Severe stridor may necessitate tracheostomy.

Recurrent laryngeal nerve injury

 Not uncommon, but is usually unilateral and often transient.
 Complete, bilateral damage may result in adducted cords and airway obstruction.
 Patients usually have cord function assessed by an ENT surgeon before

 A very large long-standing goiter may erode the tracheal cartilages.
 When the enlarged gland is removed, the trachea collapses on inspiration.

Hormonal problems

Thyroid crisis
 Now rare, as a toxic gland is rarely operated on.
 Clinical features include fever, tachycardia, dysrhythmias, abdominal pain and
 Treatment is with -blockers, iodide and steroids.
 Help from an endocrinologist/ICU should be sought.
 Mortality is extremely high.

 If all four parathyroid glands are removed, hypocalcemia will result.
 It is important to check calcium post-operatively.
 Severe hypocalcemia causes tetany.

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 Treatment initially is with 20ml of 10% calcium gluconate given slowly IV.

TUR syndrome
 Important condition that sometimes complicates transurethral resection of the

 Occurs as a result of absorption of large quantities of the 1.5% glycine irrigating
solution through open venous sinuses.
 Has an incidence of up to 15% of TURPs, and is not uncommonly fatal.

 The clinical effects are mainly due to hemodilution and hyponatremia.
 The first signs are restlessness, headache, confusion.
 Initial hemodynamic signs are a widening of the pulse pressure and increase in
SBP. This is followed by hypotension, bradycardia, dysrhythmias and, in severe
cases, cardiac arrest.
 If severe, cerebral edema with convulsions or coma, and pulmonary edema.

 Confirmed by measurement of plasma sodium. Problems are likely when the
sodium is < 120, but any significant drop should be taken significantly.
 The hemoglobin and hematocrit are usually depressed by the hemodilution.


Loop diuretics
 Furosemide 40 mg IV.
 Given that the majority of the patients are fluid overloaded and the most serious
complications (cerebral edema) are a consequence of this. However, furosemide
causes diuresis by removal of sodium which is a curious way to treat

Do nothing
 Based on the knowledge that many patients with severe hyponatremia (as low as
104 mmol/l) may be asymptomatic and spontaneously correct the problem.
 Rapid correction of hyponatremia is dangerous.

Active treatment with saline

 Give either NS or more controversially 1.8% hypertonic saline.
 The big danger is that there will be further volume loading in a patient who is
already overloaded.
 It has been recommended that the sodium level should not rise more than 2

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Stable patients
 Receive only the usual maintenance fluid; avoid dextrose or dextrose-saline
 Hesitate to treat a low hematocrit with blood transfusion unless you are sure that
a heavy blood loss took place.
 Check electrolytes regularly (q6hr).

Unstable patients
 Hemodynamic instability or convulsions should be managed in the ICU.
 The difficulties with the clinical assessment of volume status make invasive
monitoring with CVP or even Swan-Ganz catheters justified.
 Inotropes or calcium may be indicated and coagulation studies performed as DIC
is a recognized complication.

Eye problems

Corneal abrasion
 The eye is sore and red, with a gritty feeling.
 Confirm diagnosis by placing a drop of 0.5% amethocaine, followed by
fluorescein. The abrasion will take up the stain.
 Treatment consists of an eye pad and bandage, and chloramphenicol ointment.

Acute (closed angle) glaucoma)

 Severe pain in and around the eye along with nausea and vomiting.
 The cornea may be cloudy and the pupil dilated.
 Call an ophthalmologist stat
 Emergency treatment is with diuretics such as acetazolamide / Diamox 500mg or
10% mannitol.

Acute blindness
 Rare (and often transient)
 May occur due to retinal infarction from prolonged pressure on the eye, from
basilar artery spasm, acute MS or even TUR syndrome.
 Although there is no specific treatment advice from an ophthalmologist should
be urgently sought.
 In the case of retinal infarction, place a patch over the eye to decrease the
metabolic work and hence oxygen requirement of the ischemic retina.

Post-intubation problems

Sore throat
 Common
 Requires only symptomatic treatment (lozenges).

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Dental damage
 Teeth should be found
 early in-patient dental treatment should be offered

Damage to pharyngeal mucosa

 can lead to extensive surgical emphysema or retropharyngeal abscess

Damage to vocal cords

 transient hoarseness

Arytenoid dislocation
 Presents with hoarseness and odynophagia
 ENT referral indicated

Recurrent laryngeal nerve damage

 may be damaged

Musculoskeletal problems

Swollen joints

 For a single joint (especially the foot), the most likely cause postoperatively is
 Measure uric acid.
 Involve a rheumatologist
 Treat with strong NSAIDs (indomethacin 50 mg tid)

Septic arthritis
 There will be signs of infection
 Treatment is with immobilization, antibiotics and joint aspiration.

Nerve injuries
 Occur as a result of poor positioning, injection of substances into the nerve or
use of tourniquets.
 Full documentation should be made immediately a nerve injury is suspected.
 Recovery is usual, but may take months.

Anaphylactoid reactions

 Type 1 hypersensitivity reaction, or true anaphylaxis. In this type, prior
exposure to the drug is required. On the first exposure, lymphocytes produce

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specific IgE antibodies, which attach to the membranes of mast cells and
basophils. A second exposure leads to degranulation of mast cells on a massive
 Complement-mediated reactions. Here exposure leads to activation of
complement cascade which cause mast cell degranulation. Prior exposure is not

 Skin: characteristic urticarial rash or flushing usually appears rapidly
 Cardiovascular system: hypotension to total cardiovascular collapse.
Hypotension is the result of release of histamine and other vasoactive peptides
which cause widespread capillary vasodilation and increased capillary
permeability. Leakage of fluid may cause significant ECF loss. Dysrhythmias
may occur, most commonly supraventricular tachycardia.
 Bronchospasm: may be life-threatening
 Glottic edema: occasionally occurs, threatening the airway.
 Gastrointestinal: Immediately after recovery, the patient may complain of
abdominal pain, diarrhea, nausea and vomiting.
 Miscellaneous: Other effects include conduction defects, coagulation
disorders and leukopenia.


 Discontinue administration of suspected drugs, give oxygen and maintain the
 Call a cardiac arrest.
 Give epinephrine. The earlier the epinephrine given, the better the outcome.
Initial IV dose should be 0.1 mg (which is 1 m of 1 in 10,000) given in
increments of 0.1 mg.
 Give IVF stat. 1-2 liters of saline. Good venous access is required (14 or 16
gauge). Colloid solutions may be preferable if available.
 Glottic edema may require intubation or cricothyroidotomy.

 Antihistamines. The agent of choice is chlorpheniramine / Chlor-Trimeton (10-20
mg slowly IV) or diphenhyramine / Benadryl (25 - 50 mg IV/PO/IM q 6hr).
 Aminophylline may be required for persistent bronchospasm particularly in the
absence of hypotension; 5 mg/kg can be given over 20 minutes.
 Steroids have no place in immediate management. They may be given if the
reaction persists, for example hydrocortisone 200 mg IV.
 Labs: it may be desirable to take blood samples to confirm the diagnosis and
identify the agent responsible. Two EDTA (red-top) tubes should be taken
immediately after the reaction and again at 3, 6, 12 and 24 hours.
 When a drug is implicated with reasonable certainty, the patient should be
informed. Full documentation should be made. Inform the patient’s primary
care physician.

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Tracheostomy Care
 Patient’s cannot speak (except with ‘fenestrated’ tubes which are placed later in
the recovery). Make sure writing materials are available.
 Normal cough is not possible. Regular suctioning and PT are need to prevent
sputum retention.
 Dysphagia is common due to the bulk of the cuff and to poorly coordinated
swallowing. This may be partially relieved by temporarily deflating the cuff. It is
important to assess swallowing before allowing solids. Use methylene blue, ask
the patient to swallow, observe for coughing, and then examine the tracheal
aspirate for coloration.
 The presence of a foreign body is irritating and causes secretions. These may
form hard crusts and can obstruct the tube. Humidification and regular
suctioning are effective in prevention.
 Pressure necrosis of the trachea is caused by a poorly positioned tube or an
overinflated cuff. This can result in stenosis or edema which make extubation
impossible. Erosion into the anterior neck can lead to fatal hemorrhage. Always
check cuff pressure regularly and do not let it exceed 20 cmH2O.

Changing the tube

 Changing the tube can be hazardous.
 The tissue planes can shift on removing the old tube so that the tract disappears.
 A common mistake is to place the new tube too far anteriorly which results in
cannulation of the anterior mediastinum and no useful airway.
 To intubate the trachea direct the tube first posteriorly until it reaches the back
wall of the trachea (a depth of 3-4 cm) and then turn it inferiorly.
 If you are faced with an obstructed tracheostomy put out a code call.
 Check the tube for obvious blockage, then try to pass a suction catheter through

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