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3rd year - Surgery > Basics > Flashcards

Basics Flashcards

1
Q

What is the body’s endocrine response to surgery?

A

1) afferent nerve input from surgery activate sympathetic nervous system (SNS) and hypothalamus-pituitary-adrenal (HPA) axis
2) SNS and HPA alter secretion of hormones
a) SNS secrete catecholamines (epinephrine, nor-epinephrine) -> tachycardia, hypertension
b) catecholamine -> kidney secrete renin -> activation of renin angiotensin system -> sodium and water retention
c) catecholamine -> pancreas secrete glucagon -> glycolysis and hyperglycemia
d) catecholamine -> inhibition of insulin secretion by pancreas -> hyperglycemia
e) anterior pituitary secrete growth hormone -> liver secrete insulin-like growth factor (IGF) to prevent protein breakdown and promote tissue repair

f) anterior pituitary secrete adrenocorticotrophic hormone (ACTH) -> adrenal gland secrete cortisol and mineral corticoid -> cortisol contribute to hyperglycemia; mineralcorticoid cause
sodium & water retention and secretion of potassium (hypokalemia)

g) anterior pituitary also secrete beta-endorphin and prolactin -> unknown effects
h) posterior pituitary -> secrete anti-diuretic hormone (ADH) -> hypertension, water retention (hyponatremia)

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2
Q

So what is the overall result of the endocrine response of the body due to surgery?

A
  1. increased blood pressure and heart rate
  2. sodium and water retention, which usually counters peri-operative volume loss (blood loss, evaporation)
  3. electrolyte imbalance: hypokalemia, hyponatremia
  4. hyperglycemia
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3
Q

What is the body’s inflammatory response to surgery?

A

surgery as stimulus cause release of cytokines including IL-6

cytokines elicit acute phase reaction

a) liver secrete acute phase protein including C reactive protein (CRP), coagulation proteins
b) liver sequestrate cations including iron and zinc
c) liver decrease production in transport protein including albumin
d) pyrexia (fever)
e) neutrophil leukocytosis, lymphocyte differentiation

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4
Q

So what is the result of the body’s inflammatory response to surgery?

A

fever

leukocytosis

increased CRP

low albumin

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5
Q

What is done to modify the body’s endocrine and inflammatory response to surgery?

A

pre-operative optimization including proper nutrition to prevent adverse effect of stress response, hormone therapy (insulin for diabetes, cortisol for adrenal insufficiency)

anesthesia decrease stress response (SNS and HPA)

refined surgical technique (such as minimal invasive surgery) decrease inflammatory response

maintaining homeostasis peri-operative including maintaining normothermia, fluid replacement for volume loss

post-operative correction of fluid and electrolyte balance

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6
Q

Common post-operative complications

A

wound: wound infection, wound dehiscence
cardiac: myocardial infarction, hypotension
pulmonary: atelectasis

GI: acute gastric dilatation, ileus

renal: acute renal failure, volume overload, hyponatremia, hypernatremia, hypokalemia, hyperkalemia

GU: urinary retention, urosepsis

hematologic: deep vein thrombosis, pulmonary embolism, post-operative bleeding

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7
Q

Causes of immediate POD 1 post-operative fever

A

pulmonary: atelectasis
inflammatory: inflammatory reaction in response to trauma from surgery, reaction to blood products during surgery

malignant hyperthermia

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8
Q

Causes of acute POD 1-2 post-operative fever

A

pulmonary: atelectasis, aspiration pneumonitis
infection: early wound infection (Clostridium, group A streptococcus)
endocrine: Addisonian crisis, thyroid storm
inflammatory: transfusion reaction

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9
Q

Causes of subacute POD 3-7 post-operative fever

A

infection: surgical site infection, IV site infection, septic thrombophlebitis, leakage at bowel anastomosis, urinary tract infection (UTI)

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10
Q

Causes of delayed POD >8 post-operative fever

A

infection: intra-abdominal abscess, peri-rectal abscess, upper respiratory tract infection, infected seroma / biloma / hematoma, parotitis, C. difficile colitis, endocarditis
hematologic: deep vein thrombosis (DVT), pulmonary embolism (PE)

GI: cholecystitis

iatrogenic: drug fever

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11
Q

What are the 5 W’s of post op fever

A

Wind POD 1-2 (pulmonary: atelectasis, aspiration, pneumonia)

Water POD 3-5 (urinary: urinary tract infection)

Weins POD 4-6 (venous thrombosis: DVT, PE)

Wound POD 5-7 (wound: surgical site infection)

What did we do? POD >7 (iatrogenic: drug fever, IV lines related infection, reaction to blood products)

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12
Q

Risk factors for surgical site/wound infection

A

1) Procedure risk factors

procedure sterility
clean (elective, not emergent, not traumatic, no acute inflammation, respiratory / GI / biliary / GU tract not entered): low risk <1.5% of surgical site infection

clean-contaminated (elective entering of respiratory / GI / biliary / GU tract): low risk <3% of surgical site infection

contaminated (non-purulent inflammation, gross spillage from GI, entry into infected respiratory / GI / biliary / GU tract, penetrating trauma <4 hours old): medium risk 5% of
surgical site infection

dirty (purulent inflammation, pre-op perforation of respiratory / GI / biliary / GU tract, penetrating trauma >4 hours old): high risk 33-50% of surgical site infection

long procedure >2 hours long

use of drains

break in sterile technique

2) Patient risk factors
age
body habitus: obesity, malnutrition
immune suppression
radiation, chemotherapy
comorbidity: diabetes, patient with other infection

3) Wound factors
reduced blood flow, hypoxemia, hypothermia
hematoma, seroma
foreign body (drains, sutures, grafts)

4) other factors
setting: prolonged pre-operative hospitalization

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13
Q

Most common bacterial pathogens that cause post op wound infection

A 
Staphylococcus aureus
Streptococcus spp. 
Clostridium spp.
E. coli
Enterococcus
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14
Q

Clinical presentation of post op wound infection

A

post-operative fever, classically POD #3-6

wound (signs of inflammation): blancheable wound erythema, swelling / induration, pain, frank pus or purulo-sanguinous discharge, warmth

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15
Q

Local infection complications of post op wound infection

A

fistula, sinus tracts, abscess, local spread (necrotizing fasciitis)

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16
Q

Local wound healing complications of post op wound infection

A

suppressed wound healing, wound dehiscence, evisceration, hernia

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17
Q

Systemic complications of post op wound infection

A

sepsis, super-infection

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18
Q

Prevention of surgical site infection

A

1) pre-operative
pre-operative IV antibiotics (typically Cefazolin) for all surgery, typically within 1 hour pre-incision and reduced Q4H in operating room (OR)

2) operative
maintain normothermia
hyper-oxygenation
chlorhexidine and alcohol wash of surgical site and hands
meticulous surgical hand hygiene
aseptic surgical technique
delayed primary closure of incision to reduce risk of superficial surgical site infection

3) post-operative
post-operative prophylactic antibiotics for contaminated and dirty surgeries (usually intra-abdominal infection requiring surgery)

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19
Q

Management of post op wound infection

A

1) source control
re-open affected part of incision and heal by secondary intention

debride necrotic & non-viable tissue, remove any infected foreign objects

2) monitoring
wound swab for C & S

demarcation of erythem

3) antibiotics
empiric antibiotic treatment

if not involving GI tract, GU tract, perineum and groin, then treat as cellulitis with Cefazolin IV

if involvement of GI tract, GU tract, perineum or groin, then Cefazolin IV + Ciprofloxacin IV + Metronidazole IV

step down to PO when stable and tolerating PO intake

narrow down spectrum based on wound culture

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20
Q

Wound dehiscence definition

A

disruption of fascial layer, usually at wound closure site due to intact suture tearing through fascia

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21
Q

Wound dehiscence risk factors

A
  1. surgical factors:
    technical failure of closure
    patient not fully paralyzed while closing
2. local factors: 
increased intra-abdominal pressure (e.g. lung hyper-inflation, ileus, bowel obstruction, obesity)
hematoma
infection
poor blood supply
radiation
3. patient factors: 
smoking
malnutrition
connective tissue disease
immune suppression
pulmonary disease
ascites
steroids
chemotherapy
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22
Q

Wound dehiscence clinical presentation

A

presentation at typically POD #1-3

wound: serosanguinous drainage, lack of healing ridge (raised area of tissue at incision), evisceration (disruption of abdominal layers and extrusion of abdominal content)

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23
Q

Wound dehiscence treatment

A

place moist dressing over wound with binder around surgical site (e.g. around abdomen for abdominal incision)

if evisceration (surgical emergency), transfer patient to OR for operative closure using slowly absorbable suture and retention sutures

conservative management: debridement of fascial and skin margins to facilitate healing

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24
Q

Most clinically significant causes of hypotension

A
  1. Hypovolemia: intra-vascular depletion, hemorrhage
  2. Cardiogenic: myocardial ischemia / infarction, heart failure
  3. Distributive: vasodilation mainly due to vasodilators / anti-hypertensive medication, anesthesia, anaphylaxis
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25
Q

Hypotensive shock management

A

if hypotensive shock, IV crystalloid fluid resuscitation (2L NS or RL bolus)
IV fluids used with caution if suspected heart failure

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26
Q

Hemorrhagic shock management

A

consider blood transfusion and stopping source of bleeding

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27
Q

Most common post-operative pulmonary complication

A

90% due to atelectasis

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28
Q

Risk factors for post op atelectasis

A

demographics: elderly

body habits: obesity

comorbidity: COPD, smoking
surgery: thoracic or upper abdominal surgery, over-sedation, significant post-operative pain

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29
Q

pathophysiology of post op atelectasis

A

shallow breathing from anesthesia, pain, bed-rest and immobility result in collapse of parts of lung

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30
Q

Clinical presentation of post op atelectasis

A

classically presentation on POD #1

low grade post operative fever

vitals: tachycardia, tachypnea, hypoxia
respiratory: decreased local air entry, bronchial breathing, crackles

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31
Q

Post op atelectasis treatment

A

1) Prevention
smoking cessation >6 weeks pre-operative

avoid over-sedation during surgery, minimize respiratory depressant medication (e.g. opioids)

aggressive and adequate pain management

deep breathing: incentive spirometry, deep breathing & coughing, chest physiotherapy

mobility: postural changes, early ambulation

2) Treatment
implement all of the preventive strategies

supplemental oxygen for hypoxia

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32
Q

Potential post op GI complications

A

Acute gastric dilatation (aka gastroparesis)

ileus

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33
Q

Acute gastric dilatation (aka gastroparesis) definition

A

delayed gastric emptying in absence of mechanical obstruction

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34
Q

Acute gastric dilatation (aka gastroparesis) causes

A

neurologic diseases and diabetes predispose to gastroparesis

gastric (classically fundoplication) or thoracic surgery can cause (permanent or reversible) injury to vagus nerve, causing delayed gastric emptying

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35
Q

Acute gastric dilatation (aka gastroparesis) clinical presentation

A

GI: nausea, vomiting (which may contain food ingested several hours earlier), early satiety, post-prandial bloating, bloating, upper abdominal pain

abdominal exam: epigastric distention / tenderness, otherwise unremarkable exam

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36
Q

Acute gastric dilatation (aka gastroparesis) diagnosis

A

gastroparesis usually diagnosed clinically based on symptoms with mechanical obstruction ruled out by upper endoscopy or CT scan

diagnosis of delayed gastric emptying can be confirmed with scintigraphy

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37
Q

Acute gastric dilatation (aka gastroparesis) treatment

A

1st line = conservative management

conservative management for all patients
dietary modification (low in fat and fiber), frequent small meals, blenderize food if symptomatic
optimize and restore fluids and electrolytes, which may be imbalanced from vomiting
unsure blood glucose control in diabetes

2nd line = pro-kinetics
pro kinetics Metoclopramide or Domperidone administered 10-15 minutes before meals

last line = percutaneous endoscopic gastrostomy tube to decompress upper GI tract and jejunal feeding tube

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38
Q

Ileus definition

A

slowed or absent peristalsis of small and large bowels without mechanical obstruction

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39
Q

Ileus causes

A

1) Physiologic
post-operative ileus, which is a normal physiologic response to most abdominal surgeries

2) Pathologic
any metabolic or physical insult to GI tract can cause ileus
metabolic and electrolyte disturbances: hypokalemia, hyponatremia, hypo-magnesium, uraemia
drugs: opiates, psychotropic agents, anticholinergics
inflammatory: intra-abdominal inflammation, systemic sepsis
vascular: hemorrhage, intestinal ischemia

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40
Q

Ileus clinical presentation

A 
GI symptoms (similar to bowel obstruction): nausea, vomiting, PO intolerance, distended abdomen, constipation, obstipation
no inflammatory symptoms / signs / markers: no fever, no peritoneal signs, no leukocytosis
abdominal exam: absent / low bowel sounds, distended abdomen, tympanic on percussion, usually benign, soft &amp; non-tender
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41
Q

Ileus investigation

A

abdominal X-ray: distended small and large bowel, air in colon & rectum without transition zone, may have fluid levels on upright abdominal X-ray, no free air
consider CT scan if suspected obstruction to differentiate ileus from bowel obstruction

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42
Q

Ileus diagnosis

A

need to differentiate physiologic post-operative ileus from pathologic ileus and intestinal obstruction

physiologic ileus usually have full return to normal bowel function by post-operative day (POD) #3

features that suggest pathologic ileus or intestinal obstruction include
obstipation, constipation and no return of bowel function by POD #4-6
nausea / vomiting necessitating cessation of oral intake requiring IV fluid support or NG placement at POD #5

any features suggestive of pathologic ileus or intestinal obstruction should undergo further work-up and investigations for cause, which include the following

labs: CBC, electrolytes, extended electrolytes, creatinine, BUN, liver enzymes, amylase, lipase
imaging: plain abdominal X-ray

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43
Q

Ileus management

A

1) treat underlying cause / contributing factors
treat inflammation, sepsis
correct electrolyte and fluid imbalance
discontinue any medication that may contribute to ileus

2) supportive management
NG tube for decompression of upper GI tract
bowel rest with nutritional support until transition to oral feeding
replace and maintain fluid while restoring electrolyte imbalance
adequate pain management
serial abdominal physical examination and monitoring to rule out pathologic ileus / bowel obstruction

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44
Q

Causes of acute renal failure post op

A

most common causes for post-operative renal failure = pre-renal failure, acute tubular necrosis (ATN)

1) Pre-Renal
pre-renal = renal failure due to inadequate delivery of blood to kidney to be filtered where the kidney is intrinsically normal
a) Fluid loss, which is 2nd most common cause for hospitalized ARF (20% cases)
renal loss including diuretics
GI loss including vomiting, diarrhea
shock including septic shock, hypovolemic shock (including hemorrhage), obstructive shock, cariogenic shock and anaphylactic shock
hypovolemic state causing decreased effective circulating volume including congestive heart failure, cirrhosis, nephrotic syndrome
b) Vascular
thromboembolism in renal artery including catheter
aortic dissection
c) Medication
NSAID, which cause constriction of afferent arteriole
ACE inhibitor (ACEI), which cause dilatation of efferent arteriole
diuretics

2) Renal
renal = intrinsic pathology in kidney
a) Acute Tubular Necrosis (ATN), which is most common cause for hospitalized ARF (45% cases)
any prolonged pre-renal causes can eventually result in ATN
medication: Aminoglycosides, Vancomycin, Methotrexate, Cyclosporine
pigments: rhabdomyolysis, tumor lysis syndrome
IV contrast
b) Acute Interstitial Nephritis (AIN)
medication: almost all antibiotics especially beta-lactams and fluoroquinolone, NSAID, proton pump inhibitor, Phenytoin, Allopurinol, Ranitidine
infection: Legionella, Brucella, Mycoplasma, Streptococci, Leptospirosis, EBV
c) Glomerular Nephritis (GN)
nephrotic syndromes
nephritic syndromes
all nephrotic and nephrotic syndromes can be acute or chronic
d) Intrinsic renal vascular pathology
microangiopathy and hemolytic anemia (MAHA) including thrombotic thrombocytopenia Purpura-Hemolytic Ureic Syndrome (TTP/HUS), scleroderma, malignant hypertension
cholesterol emboli
vasculitis

3) Post-Renal
post-renal = structural of functional obstruction of urine flow in urinary tract causing back up of urine into kidney causing hydronephrosis and renal failure
post-renal is 3rd most common cause for hospitalized ARF (10% cases)
a) tumor
in male, benign prostatic hypertrophy (BPH) and prostate cancer
in female, cervical and ovarian cancer
bladder cancer
b) structural urologic obstructions
bladder stones
strictures along urinary tract
papillary necrosis
c) neurogenic bladder
urinary retention after surgical operation under general or spinal anesthesia

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45
Q

Acute renal failure post op definition/diagnosis

A

based on KDIGO definitions, patient diagnosed with acute renal failure if patient has any of the following:

a) urine volume <0.5ml/kg/h for 6 hours
b) increase in serum creatinine by >26.5umol/L within 48 hours
c) increase in serum creatinine by >1.5 times baseline within 7 days

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46
Q

Acute renal failure post op clinical presentation

A

1) volume overload resulting in pulmonary edema and peripheral edema
symptoms: pulmonary edema (shortness of breath), peripheral edema
signs: pulmonary edema (hypoxia, increased JVP, crackles on lung auscultation), peripheral edema (ascites, pitting peripheral edema)
2) uraemia (build up of uremic toxins)
symptoms: malaise, fatigue, nausea & vomiting, pruritus, restless leg syndrome, encephalopathy (confusion), pericarditis (pleuritic chest pain), neuropathy (glove and stocking
sensory neuropathy, wrist drop, foot drop)
signs: encephalopathy (asterixis), pericarditis (triphasic pericardial rub on auscultation of heart)
3) metabolic acidosis with increased anion gap
4) electrolyte abnormalities: hyperkalemia, hyper-phosphatemia, hypo-calcemia

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47
Q

Differentiating pre-renal vs renal vs post-renal

A

1) Rule out post-renal
put in foley catheter to relieve post-bladder obstruction
post-renal if urine outflow from catheter
pelvic and renal ultrasound
post-renal if distended bladder or hydronephrosis

2) Rule in pre-renal
history and physical exam and rule in pre-renal
history of fluid loss such as vomiting, diarrhea, diuretics or hemorrhage
physical exam of hypovolemia (low JVP, dry mucous membrane, decreased skin turgor)
history of medication causing pre-renal including NSAID, ACEI, diuretics
trial of fluid resuscitation, which should be effective for pre-renal and ineffective for renal

3) Differentiate pre-renal vs. renal based on urinalaysis
urine analysis can differentiate pre-renal vs. renal

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48
Q

Differentiating pre-renal vs renal based on urine analysis

A

Pre-renal
Urine Na concentration UNa - Low <20 mmol/L
Fractional excretion of Na (FeNa) - <1%
Fractional excretion of urea (FeUrea) - <35%
Sediment & Protein - Usually none

Renal 
Urine Na concentration UNa – Not low >20 mmol/L  
Fractional excretion of Na (FeNa) - >1%
Fractional excretion of urea (FeUrea) - >35% 
Sediment &amp; Protein – 
ATN – muddy brown casts 
AIN – WBC cast, eosinophils 
GN – proteinuria, RBC cast
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49
Q

Post renal acute renal injury urinalysis result

A

post-renal has same urine analysis results as renal

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50
Q

How to calculate FeNa

A

FeNa = (serum creatinine x urine sodium) / (serum sodium x urine creatinine)

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51
Q

How to calculate FeUrea

A

FeUrea = (serum creatinine x urine urea) / (serum urea x urine creatinine)

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52
Q

Post op acute renal failure management

A

treat underlying cause
for pre-renal or ATN, IV fluid hydration with crystalloid (NS or RL)
for post-renal, foley catheter

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53
Q

Post-op urinary retention risk factors

A 
age >50 years
history of pre-existing urinary retention
neurologic disease
history of benign prostate hypertrophy
anti-cholinergics
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54
Q

Post-op urinary retention pathophysiology

A

post-operative urinary retention can occur after any operation with general or spinal anesthesia
surgery and anesthesia cause bladder (detrusor muscle) dysfunction, urethral obstruction or failure of pelvic floor relaxation

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55
Q

Post-op urinary retention clinical presentation

A

failure to void: slow urine stream, straining to void, feeling of incomplete bladder emptying, overflow incontinence
abdominal discomfort / bladder fullness
abdominal exam: palpable bladder

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56
Q

Post-op urinary retention investigations

A

bladder ultrasound: post-void residual urine volume >100mL, which confirms urinary retention

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57
Q

Post-op urinrary retention treatment

A

foley catheter to rest bladder, then removal of foley catheter and trial of voiding

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58
Q

Post-op urosepsis pathophysiology

A

1) urinary tract infection, usually from manipulation of urinary tract during surgery or insertion of foley catheter
organisms: PPEEKS = Proteus, Pseudomonas, Enterococcus, e. coli, klebsiella, staphylococcus saprophyticus

2) urinary tract infection causing sepsis (systemic inflammatory response syndrome)

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59
Q

Post-op urosepsis clinical presentation

A

lower UTI = cystitis (infection of bladder) with symptoms of urinary urgency, frequency and dysuria without fever

upper UTI = pyelonephritis (infection of kidney) with symptoms of fever, chills, flank / back pain, nausea & vomiting as well as lower UTI symptoms (urgency, frequency, dysuria)

upper UTI may progress to urosepsis (blood infection) resulting in fever, rigours, tachycardia and hypotension

catheter UTI usually do not have lower UTI symptoms (no frequency, no dysuria, no urgency), but rather non-specific symptoms including change in mental status, fever, chills,
leukocytosis
almost all urine through catheter have bacteria, so only symptomatic bacturia are treated in patients with foley catheters

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60
Q

Post-op urosepsis investigations

A

UTI usually diagnosed based on clinical symptoms confirmed by positive routine and microscopy (R&M) urinalysis

positive urinalysis for UTI include
positive urine culture for bacteria (i.e. bacteriuria)
positive leukocyte esterase in urine
positive nitrite in urine
WBC cast on microscopy suggest upper UTI

systemic symptoms and positive blood culture with UTI symptoms suggest urosepsis

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61
Q

Post op urosepsis diagnosis

A

diagnosis requires clinical presentation confirmed by positive urinalysis

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62
Q

Post op urosepsis diagnosis

A

diagnosis requires clinical presentation confirmed by positive urinalysis

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63
Q

Post op urosepsis treatment

A

only symptomatic UTI (i.e. urinary symptoms plus positive urinalysis) requires antibiotic treatment
for cystitis, treat with any of the following:
1st line: nitrofurantoin for 5-7 days
1st line: septra (TMP/SMX) for 3 days
for pyelonephritis / urosepsis, treat with any of the following regimen:
1st line: IV gentamicin plus IV ampicillin for minimum of 7 days
1st line: IV cefotaxime for minimum of 7 days
2nd line: ciprofloxacin for minimum of 7 days
fluoroquinolone should not be used in patients with previous fluoroquinolone treatment, elderly, nursing home and post procedure UTI
if inadequate response after 3 days of antibiotic, consider alternate diagnosis (obstruction, complicated disease, resistant organism)

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64
Q

Post op bleeding pathophysiology

A

1) post-operative bleeding POD#0-2: reactionary hemorrhage
causes include
inadequate repair of blood vessels or vascular structure
unprepared injury or damage to organs or structures during course of surgery
displacement of clot in vessel or slip of ligature on blood vessel

2) post-operative bleeding POD#8-14: secondary hemorrhage
causes include
post-operative infection causing vascular damage

post-operative bleeding at any time may be due to coagulopathy, thrombocytopenia
continuous bleeding may be sustained by triad of hypothermia, coagulopathy, lactic metabolic acidosis

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65
Q

Post op bleeding clinical presentation

A

external hemorrhage: bleeding from wound

internal hemorrhage: hematoma, accumulated blood
symptoms of hematoma: increased pain
signs of hematoma: distention of tissue overlying hematoma, skin bruising / swelling, palpable mass

consequence of hypovolemia and anemia from bleeding
vitals: tachycardia, tachypnea, hypotension, orthostatic changes, decreased mental status
anemia symptoms: pre-syncope, syncope, exertional dyspnea, angina
volume depletion signs: dry mucous membrane, dry axilla, decreased skin turgor, decreased capillary refill, decreased urine output

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66
Q

Post op bleeding investigations

A

labs: CBC, blood type & cross match, INR, PTT

for suspected internal hematoma, consider ultrasound or CT to identify blood collection in body cavity

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67
Q

Post op bleeding management

A

1) Stabilize
ensure ABC’s
if suspected cervical hematoma, need reopening of operative skin incision to evacuate hematoma
if hypotension, 2 large bore IV access and IV NS bolus ~2L to maintain blood pressure
consider blood transfusion if hypotension refractory to IV fluid resuscitation, excessive bleeding, hemodynamic instability or severe anemia

2) Achieve Hemostasis
identify source of bleeding by physical examination

external hemorrhage from wound can be stopped by the following

a) compression of wound
b) opening wound, then coagulating (with silver nitrate) or suturing subcutaneous vessels

internal hemorrhage suspected based on constellation of symptoms and signs described above
a) consider ultrasound or CT scan to confirm hematoma / blood collection
b) patients who are hemodynamically unstable or have increasing abdominal girth should have surgical re-exploration to identify bleeding source and control of bleeding by
cauterization, ligation or suturing of blood vessel
c) large hematoma are drained

3) Address contributing factors
correct triad contributing to hemorrhage: coagulopathy, lactic metabolic acidosis, hypothermia

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68
Q

Risk factors for Virchow’s triad (VTE)

A 
1) Stasis i.e. immobilization
bed rest
post-surgery
long leg cast
long flights / train rides

2) Hyper-coagulable state
inherited thrombophilia: Factor V Leiden, protein C/S deficiency, anti-phospholipid antibody syndrome (APAS)
active malignancy
inflammatory disorders: systemic lupus erythematosus, inflammatory bowel disease
pregnancy, post-partum
hormone replacement / oral contraceptive pill

3) Endothelial injury
surgery
ventral venous catheter

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69
Q

DVT pathophysiology post op

A

DVT = formation of thrombus in deep veins of leg
deep veins of leg from proximal to deep: external iliac -> common femoral -> deep femoral, superficial femoral -> popliteal -> anterior & posterior tibial, peroneal

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70
Q

DVT clinical presentation

A

pain and tenderness of thigh or calf
unilateral swelling of leg with erythema and warmth
phlegmasia alba dolens = severe DVT with arterial spasm, cold & pale limb, weak pulse
phlegmasia cerulea dolens = total DVT causing severe edema, cyanosis, ischemia, venous gangrene, compartment syndrome, arterial compromise

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71
Q

DVT physical exam

A

lower leg: unilateral erythema, swelling, warmth, pitting edema, palpable cord
Homan’s sign = calf tenderness with forced dorsiflexion of foot

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72
Q

DVT investigations

A 
blood work: D-dimer
compression ultrasound (CUS) of lower limb
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73
Q

DVT diagnosis

A
  1. Well’s score for DVT as pretest probability
    Active cancer + 1
    Bed rest or major surgery within 4 weeks + 1
    Calf swelling >3cm compared to other leg +1
    Collateral non varicose superficial veins + 1
    Entire leg swollen + 1
    Tenderness along deep vein trajectory +1
    Pitting edema in symptomatic leg +1
    Paralysis, paresis or recent plaster immobilization +1
    Past history of DVT +1
    Alternative diagnosis as or more likely than DVT -2
    If total point 0-1 then DVT is unlikely (4-8%)
    If total point >1 then DVT likely (24-32%)

2) Diagnostic test ordered and interpreted based on Well’s score
Tony’s pg 11

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74
Q

DVT post op differential diagnosis

A 
MSK injury: muscle strain or tear
leg swelling in paralyzed limb
lymphangitis or lymphedema
venous insufficiency
popliteal (Baker’s) cyst
cellulitis
knee abnormality
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75
Q

DVT post op management

A

1) acute treatment
acute treatment with unfractionated heparin IV, heparin SC, low molecular weight heparin (LMWH) SC, or Fondaparinux SC
LMWH Enoxaparin 1mg/kg/dose SC Q12H
continue acute treatment until Warfarin reaches therapeutic dose INR 2-3

2) long term treatment
long term treatment with Warfarin or novel oral anticoagulant (NOAC)
start Warfarin or NOAC on first day of acute treatment with heparin, LMWH or Fondaparinux
start Warfarin at 2-5mg PO daily and increase until INR 2-3
treatment of at least 3 months for provoked DVT if underlying cause was addressed
treatment of at least 6 months and can be life time for unprovoked DVT

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76
Q

PE pathophysiology

A

DVT, a clot broke off as embolus, which then entered circulation and became lodged in pulmonary circulation (artery branches), which can have 2 potentially deadly consequences

1) dead space (ventilation but no perfusion) and hypoxemia
2) increased pulmonary vasculature resistance, causing right ventricular strain and possible failure, leading to cardiovascular collapse

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77
Q

PE Clinical Presentation

A

abrupt or gradual onset

pain on one side of chest, typically do not radiate, worse with inspiration

associated symptoms include dyspnea, syncope, cough, hemoptysis and palpitation
severe PE cause cardiovascular collapse including syncope and cardiac arrest

associated with deep vein thrombosis (leg swelling, pain)

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78
Q

PE Physical Exam

A

vital signs: fever, hypotension, tachycardia, tachypnea, low oxygen saturation (hypoxemia)
general appearance: respiratory distress
cardiovascular exam: increased JVP, peripheral edema, S3 or S4
respiratory exam: decreased breath sounds, rales
leg: signs of DVT such as swelling, erythema, warmth, palpable cord and tenderness

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79
Q

PE Investigations

A

chest X-ray: band atelectasis, decreased lung volume on affected side, pulmonary infarct / hemorrhage, edema, Hampton’s hump (wedge shape against pleura)
most PE patients will have normal chest X-ray, so chest X-ray mainly to rule out other causes including congestive heart failure, pneumonia, pneumothorax, pleural effusion

ECG: tachycardia in 40% PE cases, right ventricular strain (inverted T wave and ST depression in V1-V4) in 30% cases, right bundle branch block (RBBB) in 20% cases, S1Q3T3 (S
wave in lead I, Q wave in lead III, inverted T wave in lead III) in 20% cases, atrial fibrillation
normal ECG does not rule out PE, but can rule out STEMI and pericarditis

arterial blood gas: hypoxemia, hypocapnia, high Aa gradient, respiratory alkalosis

laboratory test: D-dimer positive

compression ultrasound (CUS) of leg: deep vein thrombosis

bed side ultrasound of heart: right ventricle dilatation

CT pulmonary angiography (CTPA) or ventilation perfusion scan (VQ scan) as confirmatory tests: can visualize embolism or decreased perfusion

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80
Q

PE diagnosis

A

Well’s score to stratify patient into low or high risk
pretest probability of PE based on Well’s score divide into low risk (<4 points) or high risk (>4 points)
Active cancer +1
Hemoptysis +1
Recent immobilization or surgery +1.5
Tachycardia (>100 bpm) +1.5
Past history of DVT or PE +1.5
Signs or symptoms of DVT +3
No alternative diagnosis as or more likely than PE +3
If total points 0-4 then PE is unlikely 6-11%
If total points >4 then PE is likely 29-40%
The signs or symptoms of DVT is based on pure clinical judgement, not the Well’s score for DVT

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81
Q

PE Diagnosis

A

Based on Well’s score
in low risk patients, PE can be ruled out with a negative D-dimer
in low risk patients with positive D-dimer, CTPA is needed to rule out PE
in high risk patients, PE is ruled in or out with CTPA
Tony’s pg 12

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82
Q

PE Differential Diagnosis

A 
myocardial ischemia / infarction
pneumonia
pneumothorax
heart failure
aortic dissection
muscle strain
viral pleuritis
interstitial lung disease
lung neoplasm
pulmonary edema
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83
Q

PE disposition

A

patients risk stratified by simplified PE Severity Index (PESI) for determining disposition

simplified PESI includes following variables, each worth 1 point:
age >80 years
history of cancer
history of heart failure or chronic lung disease
tachycardia >110 beats / min
hypotension where systolic blood pressure <100mmHg
hypoxia where oxygen saturation <90%
low risk = 0 point; high risk > 1 point

patients with low risk have low risk (1%) for 30 day mortality, thus can be discharged home to be followed up as outpatient

patients with high risk have higher risk (10%) for 30 day mortality, thus need to be admitted as inpatient

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84
Q

PE management

A

1) stabilize and address ABC (supplemental oxygen if hypoxemia, IV fluids if hypotension)

2) break clots in PE
for massive PE causing cardiovascular compromise (hypotension, tachyarrhythmia, syncope, cardiac arrest), fibrinolytics (any of the following)
tPA 100mg IV over 2 hours
Streptokinase 250,000 units IV over 30 minutes, then 100,000 units / our over 24 hours
Urokinase 4400 units / kg IV over 10 minutes, then 4400 units / kg / hour for 12 hours

for hemodynamically stable PE, anticoagulants commonly low molecular weight heparin (LMWH) for short term while starting warfarin for long term (same management as DVT,
see above)

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85
Q

What are the types of wound healing intention/closure

A

primary, secondary, tertiary

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86
Q

Indication and mechanism of primary wound closure

A

indication: clean cut wounds such as surgical wounds or acute traumatic wounds where wound edges can be brought together by external mechanism
mechanism: wound edges brought together by stitches, staples or adhesive tape

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87
Q

Indication and mechanism of secondary wound closure

A

indication: wound that cannot be cleaned or wound too large that skin cannot be brought together (e.g. ulcer)
mechanism: wound healed by body itself without any external mechanism means
require wound care

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88
Q

Indication and mechanism of tertiary wound closure (aka delayed primary closure)

A

indication: chronic or contaminated wounds where wound edges can be brought together by external mechanism
mechanism: wound left open, cleaned and observed, where it may be closed 4-5 days later (when granulation / epithelization occurred)
require wound care

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89
Q

Indication for wound care

A 
wound care only in 2nd or 3rd intention wound healing
in general, wound care indicated for any chronic non-healing wounds including surgical wounds and traumatic wounds
diabetic wounds
diabetic foot ulcer
venous leg ulcers
pressure ulcer
complex soft tissue wounds
infected wounds
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90
Q

Components and indications for medical management of wound care

A

systemic antibiotic therapy for clinically infected wound with any of the following
local signs: cellulitis (swelling, warm, erythematous, pain), lymphagitic streaking, purulence, malodor, wet gangrene, osteomyelitis
systemic signs: fever, chills, leukocytosis, nausea, hypotension, hyperglycemia, confusion

blood glucose control, especially for diabetic patients

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91
Q

Indication for debridement

A

indication for debridement include devitalized tissue, contamination, residual suture material, exudate, bowel contamination, necrotic tissue

debridement include
irrigation with isotonic normal saline as part of routine wound management and
surgical debridement with sharp instruments for removing large area of necrotic tissue or infection

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92
Q

What is used for topical therapy for wound care

A

antimicrobial cadexomer iodine (Iodosorb)

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93
Q

Different wound dressings for different wounds/wound stages

A

debridement stage: hydrogel wound dressing
granulation stage: foam and low-adherence dressing
epithelialization stage: hydrocolloid and low-adherence dressing

main classification of dressing
open: gauze moistened with saline packed into wound
semi-open: fine mesh gauze impregnanted with petroleum, paraffin wax or other ointment
semi-occlusive: films, foams, alginates, hydrocolloids, hydrogels

wound dressing typically changed daily or every other day, with exception of wound packing

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94
Q

Wound packing indication, method, care

A

wound packing usually indicated for large soft tissue defects (area of dead space between surface of intact healthy skin and wound base)
traditional gauze dressing (soaked with saline or tap water) often used to pack wounds with significant dead space
wound packing with gauze dressing requires frequent dressing changes usually 2-3 times daily such that the gauze does not completely dry out
wound dressing stopped when necrotic tissue have been removed and granulation is occurring

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95
Q

Wound closure/ coverage

A

wound closure in wound care as tertiary intention (delayed primary closure)
chronic wound should never be closed primarily, and only delayed primary closure in some cases
wounds are closed by delayed primary closure if it demonstrates progressive healing based on granulation tissue and epithelization
negative pressure wound therapy for deep wounds to reduce complexity and depth of defect prior to definitive closure
after sufficient wound care wound can be closed by
closure with suture, staple or tape
coverage with skin grafts

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96
Q

Normal wound healing for surgical wound

A

epithelialization of wound occurs 48 hours after wound closure

97
Q

Surgical wound care

A

can wash and bath POD #2-3
dressing applied in OR can be removed POD #2-4
leave wound uncovered if wound is dry
remove and change wound dressings if wound is wet or signs of infection (fever, tachycardia, pain)

remove skin sutures and staples POD #7-10
exception: removal POD #14 for incision crossing creases (e.g. groin), closure under tension, extremities or patient risk factors for poor healing (elderly, steroid use, immune
compromise)
exception: earlier removal if signs of infection

98
Q

What investigations can you order to determine if someone has low extra-cellular volume

A

Disproportionately high urea to Cr (BUN x 10 > Cr)
Urine Na concentration <20 mmol/L, FeNa <1%
Fractional excretion of urea <35%
Increased urine osmolality
Increased hematocrit
Metabolic alkalosis in mild hypovolemia and metabolic acidosis in severe hypovolemia

99
Q

Situations with low urine sodium concentration

A

Low extra-cellular volume
Heart failure
Cirrhosis

100
Q

When can urine not be interpreted for extra-cellular volume?

A

If patient is on diuretics or has kidney disease

101
Q

Hypovolemic Shock definition

A

Severe hypovolemia with >30% of intravascular volume loss causing poor perfusion of tissue

102
Q

Physical exam findings in hypovolemic shock

A 
Tachycardia 
Hypotension 
Cold, clammy extremities 
Cyanosis 
Low urine output <15 mL/h (acute kidney failure) 
Confusion
103
Q

Hypervolemia history, physical exam findings and investigations

A
  1. History – CHF
  2. Physical exam findings – high distended JVP, crackle in lung bases (pulmonary edema), ascites, leg and sacral pitting edema
  3. Investigations – pulmonary edema on CXR
104
Q

Body fluid distribution

A

60% of body weight is total water weight, but may be decreased in elderly and obese patients
2/3 of total water weight is intracellular fluid (ICF) volume
1/3 of total water weight is extracellular fluid (ECF) volume: 2/3 of extracellular fluid volume is interstitial fluid volume, 1/3 of extracellular fluid volume is intravascular volume (~7% of total body weight)

105
Q

Predominant cations

A

Sodium is predominant extracellular cation, mainly in plasma and interstitial fluid (140 mEq/L)
Potassium is predominant intracellular cation (150 mEq/L in cell)

106
Q

What exerts most o the oncotic pressure in the plasma

A

Albumin

107
Q

What regulates the intravascular volume

A

Tightly regulated by antidiuretic hormone (ADH), aldosterone and atrial natriuretic peptide (ANP)

108
Q

What are crystalloids

A

Aqueous solution of salts

109
Q

What is in D5W

A

50 g/L dextrose in water

110
Q

What is in 2/3 1/3

A

2/3 D5W and 1/3 NS = 33g glucose/L and 50 mEq Na and Cl/L

111
Q

What is in Ringer’s Lactate

A

130 mEq Na
109 mEq Cl
Small amount of K, Ca and lactate

112
Q

How much fluid is used for resuscitation to replace blood loss for crystalloids

A

Ratio of 3:1, where every 3L of NS or RL will replace 1L of blood

113
Q

How much fluid is used for resuscitation to replace blood loss for colloids

A

Every 1L of colloid will replace 1L of blood

114
Q

Where do NS, RL and D5W distribute to?

A

NS and RL increase both intravascular and interstitial volume (ECF)
D5W distributes into all body fluid compartments (2/3 ICF, 1/3 ECF)

115
Q

What are colloids

A

Aqueous solution of proteins, which theoretically increase intravascular volume over interstitial volume preferentially
Include synthetic starch solutions (Pentaspan, Volvuven, Volulyte) and blood components (albumin, pRBCs, platelets, plasma, clotting factors cryoprecipitate)

116
Q

What IV fluid is indicated for hypovolemia

A

NS or RL that will expand the extracellular fluid the most

D5W is least effective in increasing ECF because a large proportion of D5W goes into intracellular fluid

117
Q

What IV fluid is indicated for cirrhosis with hypovolemia

A

Albumin

118
Q

What IV fluid is indicated for dehydration

A

Hypotonic saline or D5W to move water into intracellular space

119
Q

Definition hypovolemia

A

Loss of water and solutes resulting in decreased ECF

120
Q

Definition dehydration

A

Loss of water resulting in decreased intracellular fluid usually presenting with hypernatremia

121
Q

IV fluid indicated for maintenance

A

0.45NS D5W or 2/3 1/3 plus 20 mEq/L KCl added to replenish both water and electrolyte losses

122
Q

IV fluid indicated for blood loss

A

Replace with crystalloid (NS or RL) and pRBC if necessary

123
Q

Normal saline indications

A

Initial fluid resuscitation
Maintenance fluid for <24h
Hypochloremia such as in vomiting, nasogastric suction
Maintenance for patients with brain injury

124
Q

Adverse effects normal saline

A 
Hyperchloremic hypernatremic non-anion gap metabolic acidosis 
Renal failure and decreased GFR 
Volume overload (heart failure, renal failure, brain injury, old age)
125
Q

Maximum of NS daily

A

0-3L daily

126
Q

Ringer’s Lactate indications

A

Initial fluid resuscitation – note that RL preferable to NS for fluid replacement and resuscitation
Maintenance fluid for <24h
Hyperchloremic metabolic acidosis

127
Q

RL relative contraindication

A

High risk for hyperkalemia (existent hyperkalemia or renal failure) – can usually be given safely to renal failure patients
Brain injury due to high risk of cerebral edema

128
Q

RL disadvantage / adverse effects

A

Not recommended to be administered with blood products

Hyperkalemia

129
Q

D5W/D10W/D50W indications

A

Maintenance fluid for patients at high risk of hypoglycemia including diabetics and infants
Dehydration (hypernatremia)

130
Q

D5W/D10W/D50W contraindications

A

High risk of hyponatremia and cerebral edema (ADH, cerebrovascular pathology, neurosurgical procedure)

131
Q

D5W/D10W/D50W adverse effects

A

Hyponatremia
Hyperglycemia
Decrease in serum osmolarity

132
Q

2/3 D5W and 1/3 NS indications

A

Maintenance fluid for 1-7 days

133
Q

2/3 D5W and 1/3 NS contraindication and adverse effects

A

Same as D5W

134
Q

Synthetic starch solution indication

A

Sometimes combined with crystalloids for large amount of resuscitation fluids to limit excessive interstitial edema from crystalloids

135
Q

Synthetic starch solution contraindication

A 
Bleeding disorders 
Sepsis 
Renal disease
Liver disease 
Volume overload
136
Q

Synthetic starch solution adverse effects

A 
Volume overload 
Coagulopathy 
Hypersensitivity reactions 
Severe renal injury 
Liver injury 
Increased blood viscosity 
Mortality 
No oxygen carrying capacity, worsen coagulation, thus are not substitute for blood products
137
Q

Maximum synthetic starch

A

~2L daily

138
Q

Albumin relative contraindication

A

High risk of volume overload

Not for trauma patients with brain injury

139
Q

What are the roles of type, screen and cross match

A

Type – confirms patient’s ABO and Rh blood groups
Screen – takes 5-10 minutes, screens patient’s blood for antibodies
Cross match – takes 45 minutes or 5 minutes in electronic cross match, which mixes patient’s blood with donor’s blood to determine presence of any reaction

140
Q

What to do if cross match is unavailable

A

O – for all children and women of child-bearing age

O+ for all adult men

141
Q

Volume 1 unit pRBC and how much will it raise hemoglobin by

A

280 mL

Will raise by ~10 g/L

142
Q

Acceptable blood loss calculation

A 
ABL = EBV x [(Hbi - Hbf) / Hbi)
ABL = acceptable blood loss in mL
EBV = estimated blood volume = blood volume mL/kg (75mL/kg for adult male and 65mL/kg for adult female) x weight kg
Hbi = pre-operative hemoglobin value g/L
Hbf = transfusion trigger hemoglobin value, which is set by clinician
143
Q

How to determine maintenance fluids

A

421 rule

Often add K 15-20 mEq/L to maintenance fluids

144
Q

How to determine fluid deficit

A

Assess volume status
Mild hypovolemia – 3% body water lost (dry axilla, mucous membranes)
Moderate hypovolemia – 6% (oliguria, orthostatic hypotension, cool peripheries, apathy)
Severe hypovolemia – 9% (profound oliguria, confusion)

145
Q

Total body water estimate

A

Estimated based on patient age and body weight
Adult male total body water is 60% body weight
Adult female total body water is 50% body weight
Elderly >65 years old total body water is 45% body weight

146
Q

Method of replacing volume deficit

A

Replace over course of 24h with half in first 8h and other half over 16h

147
Q

What causes ongoing fluid loss during surgery

A

Blood loss
Fluid moving to third space due to evaporation, tissue swelling, tissue exudates, collection in organs out of intravascular space due to surgical manipulation and capillary leakage

148
Q

How to estimate 3rd space loss during surgery

A

4/6/8 rule
4 mL/kg/h for minor surgery
6 ml/kg/h for moderate surgery
8 ml/kg/h for major procedure or trauma

149
Q

Method for replacing 3rd space loss during surgery

A

Fluid replacement of 3rd space fluid losses not recommended due to risk of fluid overload when 3rd space fluid is reintegrated into body 3 days post op

150
Q

How is blood loss estimated during surgery

A

Estimated blood loss based on visual estimate of blood in suction container, weight of surgical pads/sponges used to absorb blood

151
Q

Causes of post op fluid deficit

A

Pre-op – NPO, inadequate maintenance fluid
Peri-op – surgical bleeding, insensible water losses (evaporation), inadequate fluids, medication effect, mechanical ventilation
Post-op – decreased PO intake, inadequate maintenance fluid

152
Q

Causes of post-op fluid overload

A

Excessive fluids

Heart, renal or liver failure

153
Q

Management of post-op fluid overload

A

Decrease or discontinue IV fluids

Furosemide to excrete excessive extracellular fluids

154
Q

Causes of hyponatremia

A
  1. Low plasma osmolality
    a) Low effective circulating volume
    Hypovolemia
    Heart failure
    Cirrhosis
    Thiazide diuretics
    b) SIADH
    CNS disease including stroke, hemorrhage, infection, trauma
    Malignancy including lung cancer, pancreatic cancer and lymphoma
    Medication including DDAVP, oxytocin, cyclophosphamide, carbamazepine, morphine
    Surgery
    Lung disease including TB, pneumonia, empyema
    Hormone deficiency including adrenal insufficiency, hypothyroidism
    c) Renal failure
    d) Primary polydipsia
  2. Normal plasma osmolality
    a) High protein state (high triglycerides, multiple myeloma)
    b) Absorption of glycine, sorbitol or mannitol
  3. High plasma osmolality
    a) Hyperglycemia
    b) Alcohol intoxication with increased serum alcohol concentration
    c) Mannitol
    d) Renal failure
155
Q

Clinical presentation of hyponatremia

A

Mild to moderate – lethargy, apathy, anorexia, n/v, neurologic (headache, confusion, gait disturbance)
Severe – neurologic (seizure, disorientation, coma), respiratory (respiratory arrest)

156
Q

Signs of hyponatremia

A

Usually only with severe
Hypothermia
Abnormal sensorium, depressed reflex, seizure
Cheynes-Stokes respiration, respiratory arrest

157
Q

Causes of hyponatremia with high serum osmolality

A
  1. Hyperglycemia
  2. Azotemia (high BUN) from advanced renal failure
  3. Alcohol intoxication
158
Q

How to confirm diagnosis of azotemia from advanced renal failure

A

Calculate corrected serum osmolality = measured serum osmolality – BUN mmol/L, which should be normal

159
Q

Causes of hyponatremia with normal serum osmolality

A
  1. IV infusion of mannitol, maltose or sucrose in conjunction with IVIG
  2. Absorption of glycine, sorbitol or amniotic irrigation solution during surgery
  3. Hyperlipidemia
  4. Hyper-proteinemia in multiple myeloma
160
Q

Causes of hyponatremia with low serum osmolality

A
  1. Urine osmolality
    Urine osmolality <100 mosmol/kg and specific gravity <1.003 is an appropriate response (ADH suppression) and indicates polydipsia
    Urine osmolality >100 mosmol/kg and specific gravity >1.003 is an inappropriate response (inadequate ADH suppression) and suggests low effective circulating volume (hypovolemia, heart failure, cirrhosis) or euvolemia with SIADH, which is differentiated based on urine Na and Cl concentration
  2. Urine Na and Cl concentration
    a) Before calculating urine Na and Cl concentration, high creatinine in setting of hypervolemia suggests renal failure as cause for hyponatremia
    b) Urine Na concentration <25 mEq/L suggests low effective circulating volume
    With hypervolemia suggests heart failure or cirrhosis
    With hypovolemia suggests hypovolemia
    c) Urine Na concentration >40 mEq/L and high fractional excretion of sodium (FeNa) suggests SIADH including hormone deficiency
    d) In hypovolemic hyponatremic patients with metabolic alkalosis due to vomiting, urine Na concentration ma be >25 mEq/L but urine Cl concentration is <25 mEq/L
    e) In patients with acute kidney injury, FeNa <1% suggests effective volume depletion
161
Q

When can urine Na and Cl concentration not be interpreted

A

If patient is taking diuretics

If patient has salt wasting nephropathy

162
Q

Acute and chronic hyponatremia definitions

A

Within 24h acute, for 48h chronic

163
Q

Severity classification hyponatremia

A

Mild 130-135
Moderate 121-129
Severe 0-120

164
Q

Hyponatremia general management

A

Water restriction to 1L per day
Diagnose and treat underlying cause
Frequent monitor of urine output and serum Na

165
Q

Raising serum Na in hyponatremia indication for emergent therapy

A

Hyponatremia with severe symptoms such as seizure, obtundation
Acute hyponatremia

166
Q

Goal of hyponatremia emergent therapy

A

Increase serum Na by 4-6 mEq/L over 6h, but not exceed increase of 8 mEq/L in any given 24h period

167
Q

First sign of dangerously rapid correction of serum Na

A

High urine output >100 cc/h with dilute urine (<100 mOsm/L)

168
Q

What is used for emergent hyponatremia therapy

A

Hypertonic saline IV 3% NaCl 1-2cc/kg/h

169
Q

DDAVP indications and contraindications

A

1-2 mcg iV or SC q8h to avoid too rapid correction of serum Na
Contraindicated in patients with primary polydipsia and volume overloaded patients (heart failure, cirrhosis)

170
Q

How to manage overly rapid Na correction

A

ADH or D5W IV

171
Q

Goal of non emergent hyponatremia correction therapy

A

Slowly increase serum Na by 3-6 mEq/L within 24h

172
Q

Non emergent hyponatremia therapy

A

Normal saline IV, with furosemide if not hypovolemic
If refractory, consider Demeclocyline 300-600 mg PO BID (ADH antagonist), oral urea 30-60 g/d or slow rate of IV 3% NaCl at 10 cc/h
Additional therapy depending on underlying cause:
1. Hypovolemia – then IV normal saline (not volume overloaded, SIADH)
2. Heart failure or SIADH with urine to serum cation ratio >1, loop diuretics Furosemide
3. If SIADH with mild asymptomatic hyponatremia, oral NaCl tablets

173
Q

Causes of hypernatremia

A
  1. Unreplaced water loss – should not persist in patients who are alert, have intact thirst mechanism, have access to water (sweating, vomiting, diarrhea, urine loss)
  2. Neurogenic dysfunction – hypothalamic lesion, central diabetic insipidus (lack of ADH)
  3. Water loss into cells – severe exercise, seizure
  4. Sodium overload – intake or administration of hypertonic sodium solution
  5. Endocrine causes – Cushing’s syndrome, Hyperaldosteronism
174
Q

Clinical presentation of hypernatremia

A

Thirst
Polyuria (>1.5L urine per day)
Neurologic (altered mental status, coma, seizure, focal neurologic deficit, weakness, neuromuscular irritability, death)

175
Q

Using lab investigations to determine etiology of hypernatremia

A
  1. Volume status
    Hypervolemic (rare) – consider Cushing’s syndrome, hyperaldosteronism
    If not hypervolemic – measure urine output and osmolality
  2. Urine osmolality
    If urine is maximally concentrated (urine osmolality >600 mOsm/kg) and urine output and minimized (<500 mL/day), then unreplaced water loss, hypothalamic lesion, severe exercise/seizure or sodium overload
    a) Urine Na <25 mEq/L suggests unreplaced water loss
    b) Urine Na >100 mEq/L suggest sodium overload
    If urine is not maximally concentrated (<300 mOsm/kg) then central or nephrogenic diabetic insipidus
    a) If administration of exogenous ADH cause 50% increase in urine osmolality then central diabetic insipidus
    b) If administration does not cause 50% increase then nephrogenic diabetic insipidus or osmotic diuresis or loop diuretics
    If total urine excretion rate >1000 mOsm/day, then loop diuretics or osmotic diuresis
176
Q

Hypernatremia management

A
  1. Treat underlying cause
    Central diabetes insipidus – DDAVP
    Hypovolemia – fluid resuscitation with IV normal saline bolus
    Hypervolemia – diuretics and dialysis if renal failure to get rid of extra water
  2. Lowering sodium regimen
    Oral free water or IV dextrose
    For chronic (>48h) D5W with goal of lowering serum Na by no more than 10 mEq/L in 24h
    For acute (<48h) D5W with goal of lowering sodium 1-2 mEq/L per hour until Na 145, then reduce D5W rate
177
Q

What can too fast decrease in serum Na cause

A

Cerebral edema leading to encephalopathy with seizure and possibly permanent neurologic damage or death

178
Q

What can too fast increase in serum Na cause

A

Osmotic pontine demyelination

179
Q

Causes of hypokalemia

A
  1. Decreased intake - rare
  2. Redistribution into cells
    Metabolic alkalosis
    Insulin
    Catecholamine, beta-agonist, theophylline
    Increased blood cell production from B12 injection, folic acid supplement and GM-CSF
  3. GI loss
    Vomiting
    Diarrhea, laxative
    NG tube drainage
  4. Renal loss
    Diuretics
    Increased mineralcorticoid-aldosterone activity: exogenous steroids, Cushing’s syndrome, adrenal adenoma, Conn’s syndrome, renovascular disease, renin tumour
    Renal tubular acidosis, DKA
    Hypomagnesium
    Rare congenital renal disease: Bartter’s disease, Gitelman’s disease, Liddles syndrome
180
Q

Clinical Presentation of hypokalemia

A

Usually asymptomatic, N/V, fatigue, generalized weakness, myalgia, muscle cramps, constipation
Severe – muscle necrosis, paralysis, arrhythmia which can be deadly

181
Q

Determining hypokalemia etiology from clinical evaluation

A
  1. Most causes easily diagnosed based on history
  2. Negative history usually suggests renal loss
    a) Renal loss usually have urine K >30 mEq/day
    b) Renal loss can be differentiated based on BP and arterial or venous blood gas
    Mineral corticoid-aldosterone causes usually have hypertension
    Non mineral corticoid-aldosterone causes have normal or hypotension

Acidosis suggests DKA and renal tubular acidosis
Alkalosis suggests congenital renal tubular lesions (Bartter’s, Gitelman’s) and diuretics and vomiting, which should be ruled out by history

182
Q

Determining severity of hypokalemia

A

ECG changes are more predictive of clinical complications than serum K level

183
Q

ECG changes seen in hypokalemia

A 
Flattened or inverted T wave 
U wave (low amplitude following T wave) 
ST depression 
Prolonged QT interval 
In severe hypokalemia – prolonged PR, wide QRS, heart blocks
184
Q

Hypokalemia treatment

A
  1. Address underlying cause
    Hypo magnesium should be treated with mag sulphate IV
  2. Replace K
    Standard therapy = KCl IV or PO
    Should be done with extreme caution in following patients due to high risk of over-correction and hyperkalemia – diabetics, elderly, impaired renal function and urine output
  3. If acidosis KHCO3 IV
185
Q

Hyperkalemia causes

A
  1. Laboratory artifact – hemolysis in test tube, prolonged tourniquet, exercise, fist clenching, sample taken from vein where IV KCl is running, extreme leukocystosis >70, extreme thrombocytosis >500
  2. Increased intake – KCl PO or IV
  3. Cellular release
    Cell lysis – intravascular hemolysis, rhabdomyolysis, tumor lysis syndrome
    Insulin deficiency
    Hyperosmolar state – hyperglycemia
    Metabolic acidosis – all metabolic acidosis except for DKA and lactic acidosis
    Medication – BB, digitalis overdose, succinylcholine
  4. Decreased renal excretion of K
    Renal failure
    Decreased renin-aldosterone activity
    a) Decreased aldosterone secretion – adrenal insufficiency, ACEI/ARB, heparin, congenital adrenal hyperplasia
    b) Reduced response to aldosterone – K sparing diuretics, renal tubular disease, Pentamidine, Trimethoprim, Cyclosporine, Tacrolimus,
186
Q

Hyperkalemia Clinical Presentation

A

Usually asymptomatic, nausea, palpitation, muscle weakness, areflexia, muscle stiffness, paresthesia, ascending paralysis, hypoventilation, arrhythmia

187
Q

Determining hyperkalemia etiology from clinical evaluation

A
  1. Rule out/in lab artifact
  2. Rule out/in increased intake
  3. Determine acute vs chronic
    Acute almost always due to cell shift
    Chronic usually due to decreased renal excretion
    Can measure plasma renin activity, serum aldosterone and serum cortisol to differentiate decreased aldosterone secretion vs decreased response to aldosterone
    a) Normal plasma renin activity and low serum aldosterone suggest decreased aldosterone secretion
    b) Normal plasma renin activity and normal serum aldosterone suggest reduced response to aldosterone
188
Q

Hyperkalemia ECG changes

A

Changes do not correlate with serum K, but predicts cardiotoxicity
Peaked and narrow T waves, usually symmetric, taller than QRS and >5 squares
Decreased amplitude and eventual loss of P wave
Prolonged PR
Widened QRS eventually merging with T wave
Arrhythmia such as AV block, V fib, asystole

189
Q

Hyperkalemia management

A
  1. Lower K
    Emergency therapy if ECG changes or patient symptomatic
    a) If ECG changes Calcium gluconate 1-2 amps 10 mL of 10% solution IV to stabilize cardiac membrane, which lasts 30-60 mins

b) Cell shift
Shift K into cells with insulin (with amp D50W) , beta-agonist and bicarbonate, thereby decreasing serum K

c) Eliminate K
If kidney function intact, furosemide 40 mg IV (+ NS bolus PRN)
If life threatening hyperkalemia unresponsive to therapy or renal failure, dialysis

  1. Address underlying cause
190
Q

Risk of using resins (calcium resinous or sodium polystyrene sultanate Kayexalate) to increase bowel excretion of K

A

Risk of colon necrosis

191
Q

Hypokalemia definition

A

<3.5 mEq/L

192
Q

Hyperkalemia definition

A

> 5 mEq/L

193
Q

Hypocalcemia definition

A

Total corrected Ca <2.25 mmol/L

194
Q

Causes of Hypocalcemia

A
  1. Low PTH
    a) Hypoparathyroidism
    b) Hypomagnesemia
    c) Hemochromatosis
  2. Vitamin D related
    a) Deficiency
    b) Renal, vitamin D dependent rickets
    c) Vitamin D resistant rickets
  3. Other
    a) PTH resistance (pseudohypoparathyroidism)
    b) Medication – calcitonin, loop diuretics including furosemide
    c) Acute pancreatitis
195
Q

Hypocalcemia clinical presentation

A
  1. Acute
    Neurologic – delirium, psychiatric symptoms, paresthesia, hyperreflexia, tetany
    Trousseau sign
    Chvostek’s sign
  2. Chronic
    Neurologic – seizure, psychosis, Parkinson’s dystonia, hemiballismus, papilledema, pseudotumour cerebri
    Cardiac – prolonged QT
    GI – steatorrhea
    Skin – dry, scaling, alopecia, brittle and transversely fissure nails, candidiasis
    Eye – cataract
    MSK – lethargy, generalized muscle weakness and wasting
196
Q

What is Trousseau sign

A

Trousseau sign: tetany of hand and forearm resulting in flexion of wrist and MCP as well as extension of DIP and PIP when blood pressure cuff is inflated

197
Q

What is Chvostek’s sign

A

Chvostek’s sign: tetany of facial nerve (CN VII) when tapped at jaw angle, resulting in twitch of nose or lips

198
Q

Diagnostic approach to hypocalcemia

A

See Tony’s pg 24

199
Q

Hypocalcemia treatment

A

Mild / asymptomatic hypocalcemia with ionized Ca >0.8mmol/L, increase dietary Ca by 1000mg / day
acute / symptomatic hypocalcemia with ionized Ca <0.7mmol/L, IV Calcium Gluconate 1-2g over 10-20 minutes followed by slow infusion with goal of increasing Ca to low normal range
2mmol/L
treat hypo magnesium and low vitamin D

200
Q

Hypercalcemia definition

A

Total corrected Ca >2.62 mmol/L or ionized Ca >1.35

201
Q

How to calculate total corrected calcium

A

Measured Ca + 0.02 (40 – albumin)

Ie for every decrease in albumin by 10 there is an increase in Ca by 0.2

202
Q

Causes of hypercalcemia

A

Primary hyperparathyroidism and malignancy account for >90% of hypercalcemia cases
1. Primary hyperparathyroidism
Parathyroid adenoma, hyperplasia, carcinoma
2. Tertiary hyperparathyroidism
Secondary hyperparathyroidism – increased PTH in response to hypocalcemia due to renal failure
Tertiary hyperparathyroidism – increased PTH after prolonged 2o due to renal failure
3. Malignancy
Skeletal, hematologic, para-neoplastic syndrome (PTHrP)
4. Vitamin D related
Excessive intake of vitamin D
Excessive calcitriol
Granulaomatous disease: TB, sarcoid, lymphoma
5. High bone turn over
Immobilization
Vitamin A intoxication
Hyperthryoidism
Paget’s disease
6. Medication
Thiazide diuretics
Theophylline
Estrogen, Tamoxifen
Lithium

203
Q

Diagnostic approach to hypercalcemia

A

Pg 24 Tony’s

204
Q

Hypercalcemia clinical presentation

A

Moans (abdominal pain), bones (bony pain), stones (nephrolithiasis), psychiatric overtones (psychosis)
Cardiac – hypertension, arrhythmia, short QT
GI – n/v, anorexia, abdominal pain, constipation, PUD, pancreatitis
Renal – polyuria, polydipsia, nephrolithiasis, renal failure
MSK – weakness, bony pain, gout, pseudogout, chondrocalcinosis
Psychiatric – confusion, cognitive dysfunction, psychosis
Neurologic – hypotonia, hypo-reflexia, myopathy, paresis

205
Q

What is a hypercalcemia crisis

A

Total corrected Ca >4mmol/L presenting with oliguria/anuria and mental status change, which is a medical emergency requiring immediate treatment

206
Q

Acute management of hypercalcemia

A
  1. Volume expansion – NS for urine output at 100-150 ml/h (loop diuretics if renal or heart failure)
  2. Lower calcium level
    Calcitonin to transiently decrease
    Bisphosphonate Pamidronate
    If vit D toxicity or granulomatous disease or hematologic malignancy  Prednisone
    If severe malignancy associated hypercalcemia and renal insufficiency/heart failure  dialysis
207
Q

Hypophosphatemia definition

A

PO4 <2.6 mg/dL

208
Q

Hypophosphatemia causes

A 
Glucose loading 
Respiratory alkalosis 
Sepsis 
DKA 
Decreased absorption of phosphate
209
Q

Hypophosphatemia clinical presentation

A

Usually asymptomatic, but may cause anemia, CHF exacerbation, weakness, shift of oxyghemoglobin curve to the left

210
Q

Hypophosphatemia management

A

if PO4 <2mg/dL, oral replacement with Neutra-Phos or K-Phos 1200-1500mg PO daily
if PO4 <1mg/dL, IV replacement with KPO4 IV 0.08-0.16mmol/kg IV over 6 hours

211
Q

Hyperphosphatemia definition

A

POV >4.8 mg/dL

212
Q

Hyperphosphatemia causes

A

Renal failure

Tumour necrosis

213
Q

Hyperphosphatemia clinical presentation

A

usually asymptomatic

214
Q

Hyperphosphatemia management

A

Sucralfate 1 g PO QID

Hemodialysis

215
Q

Hypomagnesemia definition

A

Mg <1.5 mg/dl

216
Q

Hypomagnesemia causes

A

medication: diuretics (Furosemide), aminoglycosides, cisplatin
diarrhea
diabetes
alcoholism

217
Q

Hypomagnesemia clinical presentation

A

low Na, K, Ca or PO4
arrhythmia
seizure

218
Q

Hypomagnesemia management

A

oral replacement: Magnesium oxide 400mg PO daily or Magnesium gluconate 500mg PO daily
IV replacement: Magnesium sulphate 1-2g over 1 hour infusion

219
Q

Hypermagnesemia definition

A

> 2.5 mg/dL

220
Q

Hypermagnesemia cause

A

Hemolysis

Renal failure

221
Q

Hypermagnesemia clinical presentation

A

hyporeflexia (Mg = 4mg/dL) -> complete heart block (10mg/dL) -> cardiac arrest (13mg/dL)

222
Q

Hypermagnesemia management

A

Calcium gluconate 1g IV over 2-3 minutes to stabilize cardiac membrane
volume replacement and Furosemide to excrete Mg in urine
hemodialysis if severe hypermagnesemia

223
Q

Indications for intubation

A

Loss of gag/cough reflex with risk of massive aspiration, most commonly due to decreased LOC GCS<8
Existent or anticipated airway obstruction
Requirement for mechanical ventilation
a) Failure to ventilate PaCO2 >60 mmHg
b) Failure to oxygenate PaO2 <70 mmHg on 70% FiO2
c) Impending failure to ventilate and/or oxygenate (respiratory rate >30, pH <7.2)

224
Q

Alternative to endotracheal intubation if patient is conscious

A

Nasotracheal intubation

225
Q

Hypoxemia oxygenation intervention order

A

In order of increasing FiO2

Nasal prongs  simple face mask non-breather masks  CPAP/BiPAP mechanical ventilation

226
Q

What should you do for someone not ventilating

A

Lack of ventilation requires bag-valve mask or assisted ventilation (CPAP, BiPAP) or mechanical ventilation

227
Q

Differentiate the 4 classes of hemorrhagic shock

A

Class 1 – pulse <100
Class 2 – pulse >100, cap refill decreased
Class 3 – BP decreased, altered level of consciousness
Class 4 – obtunded/loss of consciousness

228
Q

How to resuscitate the 4 classes of hemorrhagic shock

A 
Crystalloid for class I and II 
Crystalloid + blood for class III and IV
229
Q

What is an adequate IV fluid challenge

A

2L, where patient who is still hypotensive and tachycardic after challenge requires blood transfusion and investigation/management for ongoing bleeding

230
Q

Procedure of giving blood transfusion

A

Start with 2 units of RBCs

Add plasma/platelets after giving 6 units of RBC

231
Q

Role of vasopressor in resuscitation of trauma patients

A

None – may mask vitals

232
Q

Resuscitation end points (ie return to normal perfusion)

A
  1. Restoration of normal vital signs
  2. Tissue perfusion (MAP 65 mm Hg plus; CVP 8-12 mm Hg when central access available)
  3. Oxygen transport (normal lactate; mixed venous oxyhemoglobin saturation SvO2 >65% if pulmonary artery catheter used; central venous (SVC) oxyhemoglobin saturation ScvO2 70%+ when central access available
  4. End-organ perfusion (normal mental status, urine output >0.5-1 cc/kg/h, warm skin with normal cap refill)
233
Q

How to calculate MAP

A

[2 x diastolic + systolic] /3

234
Q

GCS Score

A 
Eyes open 
4- spontaneously 
3- to voice 
2- to pain 
1- no response 
Best verbal response 
Answers questions appropriately 5 
Confused, disoriented 4 
Inappropriate words 3
Incomprehensible sounds 2 
No verbal response 1
Best motor response 
Obeys commands 6 
Localizes to pain 5 
Withdraws from pain 4 
Decorticate (flexion) 3 
Decerebrate (extension) 2
No response 1
235
Q

AVPU score

A

Best response of patient awake spontaneously, responds to voice, responds to pain or unresponsive

236
Q

What history should be taken in a trauma situation

A 
SAMPLE 
Signs and symptoms 
Allergies 
Medication 
Past medical history 
Last meal 
Events related to injury
237
Q

What is Cushing reflex

A

Seen in increased ICP

Hypertension, bradycardia, irregular respiratory rate

238
Q

Contraindication to NG tube insertion

A

Suspected basal skull fracture

239
Q

Why does metabolic alkalosis occur with hypovolemia

A

Pre-renal acute renal injury inhibits the kidney’s ability to excrete bicarb

3rd year - Surgery (13 decks)

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