Basics Flashcards
What is the body’s endocrine response to surgery?
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)
So what is the overall result of the endocrine response of the body due to surgery?
- increased blood pressure and heart rate
- sodium and water retention, which usually counters peri-operative volume loss (blood loss, evaporation)
- electrolyte imbalance: hypokalemia, hyponatremia
- hyperglycemia
What is the body’s inflammatory response to surgery?
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
So what is the result of the body’s inflammatory response to surgery?
fever
leukocytosis
increased CRP
low albumin
What is done to modify the body’s endocrine and inflammatory response to surgery?
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
Common post-operative complications
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
Causes of immediate POD 1 post-operative fever
pulmonary: atelectasis
inflammatory: inflammatory reaction in response to trauma from surgery, reaction to blood products during surgery
malignant hyperthermia
Causes of acute POD 1-2 post-operative fever
pulmonary: atelectasis, aspiration pneumonitis
infection: early wound infection (Clostridium, group A streptococcus)
endocrine: Addisonian crisis, thyroid storm
inflammatory: transfusion reaction
Causes of subacute POD 3-7 post-operative fever
infection: surgical site infection, IV site infection, septic thrombophlebitis, leakage at bowel anastomosis, urinary tract infection (UTI)
Causes of delayed POD >8 post-operative fever
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
What are the 5 W’s of post op fever
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)
Risk factors for surgical site/wound infection
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
Most common bacterial pathogens that cause post op wound infection
Staphylococcus aureus Streptococcus spp. Clostridium spp. E. coli Enterococcus
Clinical presentation of post op wound infection
post-operative fever, classically POD #3-6
wound (signs of inflammation): blancheable wound erythema, swelling / induration, pain, frank pus or purulo-sanguinous discharge, warmth
Local infection complications of post op wound infection
fistula, sinus tracts, abscess, local spread (necrotizing fasciitis)
Local wound healing complications of post op wound infection
suppressed wound healing, wound dehiscence, evisceration, hernia
Systemic complications of post op wound infection
sepsis, super-infection
Prevention of surgical site infection
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)
Management of post op wound infection
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
Wound dehiscence definition
disruption of fascial layer, usually at wound closure site due to intact suture tearing through fascia
Wound dehiscence risk factors
- 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
Wound dehiscence clinical presentation
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)
Wound dehiscence treatment
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
Most clinically significant causes of hypotension
- Hypovolemia: intra-vascular depletion, hemorrhage
- Cardiogenic: myocardial ischemia / infarction, heart failure
- Distributive: vasodilation mainly due to vasodilators / anti-hypertensive medication, anesthesia, anaphylaxis
Hypotensive shock management
if hypotensive shock, IV crystalloid fluid resuscitation (2L NS or RL bolus)
IV fluids used with caution if suspected heart failure
Hemorrhagic shock management
consider blood transfusion and stopping source of bleeding
Most common post-operative pulmonary complication
90% due to atelectasis
Risk factors for post op atelectasis
demographics: elderly
body habits: obesity
comorbidity: COPD, smoking
surgery: thoracic or upper abdominal surgery, over-sedation, significant post-operative pain
pathophysiology of post op atelectasis
shallow breathing from anesthesia, pain, bed-rest and immobility result in collapse of parts of lung
Clinical presentation of post op atelectasis
classically presentation on POD #1
low grade post operative fever
vitals: tachycardia, tachypnea, hypoxia
respiratory: decreased local air entry, bronchial breathing, crackles
Post op atelectasis treatment
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
Potential post op GI complications
Acute gastric dilatation (aka gastroparesis)
ileus
Acute gastric dilatation (aka gastroparesis) definition
delayed gastric emptying in absence of mechanical obstruction
Acute gastric dilatation (aka gastroparesis) causes
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
Acute gastric dilatation (aka gastroparesis) clinical presentation
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
Acute gastric dilatation (aka gastroparesis) diagnosis
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
Acute gastric dilatation (aka gastroparesis) treatment
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
Ileus definition
slowed or absent peristalsis of small and large bowels without mechanical obstruction
Ileus causes
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
Ileus clinical presentation
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 & non-tender
Ileus investigation
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
Ileus diagnosis
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
Ileus management
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
Causes of acute renal failure post op
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
Acute renal failure post op definition/diagnosis
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
Acute renal failure post op clinical presentation
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
Differentiating pre-renal vs renal vs post-renal
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
Differentiating pre-renal vs renal based on urine analysis
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 & Protein – ATN – muddy brown casts AIN – WBC cast, eosinophils GN – proteinuria, RBC cast
Post renal acute renal injury urinalysis result
post-renal has same urine analysis results as renal
How to calculate FeNa
FeNa = (serum creatinine x urine sodium) / (serum sodium x urine creatinine)
How to calculate FeUrea
FeUrea = (serum creatinine x urine urea) / (serum urea x urine creatinine)
Post op acute renal failure management
treat underlying cause
for pre-renal or ATN, IV fluid hydration with crystalloid (NS or RL)
for post-renal, foley catheter
Post-op urinary retention risk factors
age >50 years history of pre-existing urinary retention neurologic disease history of benign prostate hypertrophy anti-cholinergics
Post-op urinary retention pathophysiology
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
Post-op urinary retention clinical presentation
failure to void: slow urine stream, straining to void, feeling of incomplete bladder emptying, overflow incontinence
abdominal discomfort / bladder fullness
abdominal exam: palpable bladder
Post-op urinary retention investigations
bladder ultrasound: post-void residual urine volume >100mL, which confirms urinary retention
Post-op urinrary retention treatment
foley catheter to rest bladder, then removal of foley catheter and trial of voiding
Post-op urosepsis pathophysiology
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)
Post-op urosepsis clinical presentation
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
Post-op urosepsis investigations
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
Post op urosepsis diagnosis
diagnosis requires clinical presentation confirmed by positive urinalysis
Post op urosepsis diagnosis
diagnosis requires clinical presentation confirmed by positive urinalysis
Post op urosepsis treatment
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)
Post op bleeding pathophysiology
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
Post op bleeding clinical presentation
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
Post op bleeding investigations
labs: CBC, blood type & cross match, INR, PTT
for suspected internal hematoma, consider ultrasound or CT to identify blood collection in body cavity
Post op bleeding management
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
Risk factors for Virchow’s triad (VTE)
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
DVT pathophysiology post op
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
DVT clinical presentation
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
DVT physical exam
lower leg: unilateral erythema, swelling, warmth, pitting edema, palpable cord
Homan’s sign = calf tenderness with forced dorsiflexion of foot
DVT investigations
blood work: D-dimer compression ultrasound (CUS) of lower limb
DVT diagnosis
- 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
DVT post op differential diagnosis
MSK injury: muscle strain or tear leg swelling in paralyzed limb lymphangitis or lymphedema venous insufficiency popliteal (Baker’s) cyst cellulitis knee abnormality
DVT post op management
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
PE pathophysiology
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
PE Clinical Presentation
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)
PE Physical Exam
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
PE Investigations
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
PE diagnosis
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
PE Diagnosis
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
PE Differential Diagnosis
myocardial ischemia / infarction pneumonia pneumothorax heart failure aortic dissection muscle strain viral pleuritis interstitial lung disease lung neoplasm pulmonary edema
PE disposition
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
PE management
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)
What are the types of wound healing intention/closure
primary, secondary, tertiary
Indication and mechanism of primary wound closure
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
Indication and mechanism of secondary wound closure
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
Indication and mechanism of tertiary wound closure (aka delayed primary closure)
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
Indication for wound care
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
Components and indications for medical management of wound care
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
Indication for debridement
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
What is used for topical therapy for wound care
antimicrobial cadexomer iodine (Iodosorb)
Different wound dressings for different wounds/wound stages
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
Wound packing indication, method, care
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
Wound closure/ coverage
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
Normal wound healing for surgical wound
epithelialization of wound occurs 48 hours after wound closure
Surgical wound care
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
What investigations can you order to determine if someone has low extra-cellular volume
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
Situations with low urine sodium concentration
Low extra-cellular volume
Heart failure
Cirrhosis
When can urine not be interpreted for extra-cellular volume?
If patient is on diuretics or has kidney disease
Hypovolemic Shock definition
Severe hypovolemia with >30% of intravascular volume loss causing poor perfusion of tissue
Physical exam findings in hypovolemic shock
Tachycardia Hypotension Cold, clammy extremities Cyanosis Low urine output <15 mL/h (acute kidney failure) Confusion
Hypervolemia history, physical exam findings and investigations
- History – CHF
- Physical exam findings – high distended JVP, crackle in lung bases (pulmonary edema), ascites, leg and sacral pitting edema
- Investigations – pulmonary edema on CXR
Body fluid distribution
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)
Predominant cations
Sodium is predominant extracellular cation, mainly in plasma and interstitial fluid (140 mEq/L)
Potassium is predominant intracellular cation (150 mEq/L in cell)
What exerts most o the oncotic pressure in the plasma
Albumin
What regulates the intravascular volume
Tightly regulated by antidiuretic hormone (ADH), aldosterone and atrial natriuretic peptide (ANP)
What are crystalloids
Aqueous solution of salts
What is in D5W
50 g/L dextrose in water
What is in 2/3 1/3
2/3 D5W and 1/3 NS = 33g glucose/L and 50 mEq Na and Cl/L
What is in Ringer’s Lactate
130 mEq Na
109 mEq Cl
Small amount of K, Ca and lactate
How much fluid is used for resuscitation to replace blood loss for crystalloids
Ratio of 3:1, where every 3L of NS or RL will replace 1L of blood
How much fluid is used for resuscitation to replace blood loss for colloids
Every 1L of colloid will replace 1L of blood
Where do NS, RL and D5W distribute to?
NS and RL increase both intravascular and interstitial volume (ECF)
D5W distributes into all body fluid compartments (2/3 ICF, 1/3 ECF)
What are colloids
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)
What IV fluid is indicated for hypovolemia
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
What IV fluid is indicated for cirrhosis with hypovolemia
Albumin
What IV fluid is indicated for dehydration
Hypotonic saline or D5W to move water into intracellular space
Definition hypovolemia
Loss of water and solutes resulting in decreased ECF
Definition dehydration
Loss of water resulting in decreased intracellular fluid usually presenting with hypernatremia
IV fluid indicated for maintenance
0.45NS D5W or 2/3 1/3 plus 20 mEq/L KCl added to replenish both water and electrolyte losses
IV fluid indicated for blood loss
Replace with crystalloid (NS or RL) and pRBC if necessary
Normal saline indications
Initial fluid resuscitation
Maintenance fluid for <24h
Hypochloremia such as in vomiting, nasogastric suction
Maintenance for patients with brain injury
Adverse effects normal saline
Hyperchloremic hypernatremic non-anion gap metabolic acidosis Renal failure and decreased GFR Volume overload (heart failure, renal failure, brain injury, old age)
Maximum of NS daily
0-3L daily
Ringer’s Lactate indications
Initial fluid resuscitation – note that RL preferable to NS for fluid replacement and resuscitation
Maintenance fluid for <24h
Hyperchloremic metabolic acidosis
RL relative contraindication
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
RL disadvantage / adverse effects
Not recommended to be administered with blood products
Hyperkalemia
D5W/D10W/D50W indications
Maintenance fluid for patients at high risk of hypoglycemia including diabetics and infants
Dehydration (hypernatremia)
D5W/D10W/D50W contraindications
High risk of hyponatremia and cerebral edema (ADH, cerebrovascular pathology, neurosurgical procedure)
D5W/D10W/D50W adverse effects
Hyponatremia
Hyperglycemia
Decrease in serum osmolarity
2/3 D5W and 1/3 NS indications
Maintenance fluid for 1-7 days
2/3 D5W and 1/3 NS contraindication and adverse effects
Same as D5W
Synthetic starch solution indication
Sometimes combined with crystalloids for large amount of resuscitation fluids to limit excessive interstitial edema from crystalloids
Synthetic starch solution contraindication
Bleeding disorders Sepsis Renal disease Liver disease Volume overload
Synthetic starch solution adverse effects
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
Maximum synthetic starch
~2L daily
Albumin relative contraindication
High risk of volume overload
Not for trauma patients with brain injury
What are the roles of type, screen and cross match
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
What to do if cross match is unavailable
O – for all children and women of child-bearing age
O+ for all adult men
Volume 1 unit pRBC and how much will it raise hemoglobin by
280 mL
Will raise by ~10 g/L
Acceptable blood loss calculation
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
How to determine maintenance fluids
421 rule
Often add K 15-20 mEq/L to maintenance fluids
How to determine fluid deficit
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)
Total body water estimate
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
Method of replacing volume deficit
Replace over course of 24h with half in first 8h and other half over 16h
What causes ongoing fluid loss during surgery
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
How to estimate 3rd space loss during surgery
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
Method for replacing 3rd space loss during surgery
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
How is blood loss estimated during surgery
Estimated blood loss based on visual estimate of blood in suction container, weight of surgical pads/sponges used to absorb blood
Causes of post op fluid deficit
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
Causes of post-op fluid overload
Excessive fluids
Heart, renal or liver failure
Management of post-op fluid overload
Decrease or discontinue IV fluids
Furosemide to excrete excessive extracellular fluids
Causes of hyponatremia
- 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 - Normal plasma osmolality
a) High protein state (high triglycerides, multiple myeloma)
b) Absorption of glycine, sorbitol or mannitol - High plasma osmolality
a) Hyperglycemia
b) Alcohol intoxication with increased serum alcohol concentration
c) Mannitol
d) Renal failure
Clinical presentation of hyponatremia
Mild to moderate – lethargy, apathy, anorexia, n/v, neurologic (headache, confusion, gait disturbance)
Severe – neurologic (seizure, disorientation, coma), respiratory (respiratory arrest)
Signs of hyponatremia
Usually only with severe
Hypothermia
Abnormal sensorium, depressed reflex, seizure
Cheynes-Stokes respiration, respiratory arrest
Causes of hyponatremia with high serum osmolality
- Hyperglycemia
- Azotemia (high BUN) from advanced renal failure
- Alcohol intoxication
How to confirm diagnosis of azotemia from advanced renal failure
Calculate corrected serum osmolality = measured serum osmolality – BUN mmol/L, which should be normal
Causes of hyponatremia with normal serum osmolality
- IV infusion of mannitol, maltose or sucrose in conjunction with IVIG
- Absorption of glycine, sorbitol or amniotic irrigation solution during surgery
- Hyperlipidemia
- Hyper-proteinemia in multiple myeloma
Causes of hyponatremia with low serum osmolality
- 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 - 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
When can urine Na and Cl concentration not be interpreted
If patient is taking diuretics
If patient has salt wasting nephropathy
Acute and chronic hyponatremia definitions
Within 24h acute, for 48h chronic
Severity classification hyponatremia
Mild 130-135
Moderate 121-129
Severe 0-120
Hyponatremia general management
Water restriction to 1L per day
Diagnose and treat underlying cause
Frequent monitor of urine output and serum Na
Raising serum Na in hyponatremia indication for emergent therapy
Hyponatremia with severe symptoms such as seizure, obtundation
Acute hyponatremia
Goal of hyponatremia emergent therapy
Increase serum Na by 4-6 mEq/L over 6h, but not exceed increase of 8 mEq/L in any given 24h period
First sign of dangerously rapid correction of serum Na
High urine output >100 cc/h with dilute urine (<100 mOsm/L)
What is used for emergent hyponatremia therapy
Hypertonic saline IV 3% NaCl 1-2cc/kg/h
DDAVP indications and contraindications
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)
How to manage overly rapid Na correction
ADH or D5W IV
Goal of non emergent hyponatremia correction therapy
Slowly increase serum Na by 3-6 mEq/L within 24h
Non emergent hyponatremia therapy
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
Causes of hypernatremia
- Unreplaced water loss – should not persist in patients who are alert, have intact thirst mechanism, have access to water (sweating, vomiting, diarrhea, urine loss)
- Neurogenic dysfunction – hypothalamic lesion, central diabetic insipidus (lack of ADH)
- Water loss into cells – severe exercise, seizure
- Sodium overload – intake or administration of hypertonic sodium solution
- Endocrine causes – Cushing’s syndrome, Hyperaldosteronism
Clinical presentation of hypernatremia
Thirst
Polyuria (>1.5L urine per day)
Neurologic (altered mental status, coma, seizure, focal neurologic deficit, weakness, neuromuscular irritability, death)
Using lab investigations to determine etiology of hypernatremia
- Volume status
Hypervolemic (rare) – consider Cushing’s syndrome, hyperaldosteronism
If not hypervolemic – measure urine output and osmolality - 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
Hypernatremia management
- 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 - 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
What can too fast decrease in serum Na cause
Cerebral edema leading to encephalopathy with seizure and possibly permanent neurologic damage or death
What can too fast increase in serum Na cause
Osmotic pontine demyelination
Causes of hypokalemia
- Decreased intake - rare
- Redistribution into cells
Metabolic alkalosis
Insulin
Catecholamine, beta-agonist, theophylline
Increased blood cell production from B12 injection, folic acid supplement and GM-CSF - GI loss
Vomiting
Diarrhea, laxative
NG tube drainage - 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
Clinical Presentation of hypokalemia
Usually asymptomatic, N/V, fatigue, generalized weakness, myalgia, muscle cramps, constipation
Severe – muscle necrosis, paralysis, arrhythmia which can be deadly
Determining hypokalemia etiology from clinical evaluation
- Most causes easily diagnosed based on history
- 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
Determining severity of hypokalemia
ECG changes are more predictive of clinical complications than serum K level
ECG changes seen in hypokalemia
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
Hypokalemia treatment
- Address underlying cause
Hypo magnesium should be treated with mag sulphate IV - 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 - If acidosis KHCO3 IV
Hyperkalemia causes
- 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
- Increased intake – KCl PO or IV
- 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 - 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,
Hyperkalemia Clinical Presentation
Usually asymptomatic, nausea, palpitation, muscle weakness, areflexia, muscle stiffness, paresthesia, ascending paralysis, hypoventilation, arrhythmia
Determining hyperkalemia etiology from clinical evaluation
- Rule out/in lab artifact
- Rule out/in increased intake
- 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
Hyperkalemia ECG changes
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
Hyperkalemia management
- 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
- Address underlying cause
Risk of using resins (calcium resinous or sodium polystyrene sultanate Kayexalate) to increase bowel excretion of K
Risk of colon necrosis
Hypokalemia definition
<3.5 mEq/L
Hyperkalemia definition
> 5 mEq/L
Hypocalcemia definition
Total corrected Ca <2.25 mmol/L
Causes of Hypocalcemia
- Low PTH
a) Hypoparathyroidism
b) Hypomagnesemia
c) Hemochromatosis - Vitamin D related
a) Deficiency
b) Renal, vitamin D dependent rickets
c) Vitamin D resistant rickets - Other
a) PTH resistance (pseudohypoparathyroidism)
b) Medication – calcitonin, loop diuretics including furosemide
c) Acute pancreatitis
Hypocalcemia clinical presentation
- Acute
Neurologic – delirium, psychiatric symptoms, paresthesia, hyperreflexia, tetany
Trousseau sign
Chvostek’s sign - 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
What is Trousseau sign
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
What is Chvostek’s sign
Chvostek’s sign: tetany of facial nerve (CN VII) when tapped at jaw angle, resulting in twitch of nose or lips
Diagnostic approach to hypocalcemia
See Tony’s pg 24
Hypocalcemia treatment
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
Hypercalcemia definition
Total corrected Ca >2.62 mmol/L or ionized Ca >1.35
How to calculate total corrected calcium
Measured Ca + 0.02 (40 – albumin)
Ie for every decrease in albumin by 10 there is an increase in Ca by 0.2
Causes of hypercalcemia
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
Diagnostic approach to hypercalcemia
Pg 24 Tony’s
Hypercalcemia clinical presentation
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
What is a hypercalcemia crisis
Total corrected Ca >4mmol/L presenting with oliguria/anuria and mental status change, which is a medical emergency requiring immediate treatment
Acute management of hypercalcemia
- Volume expansion – NS for urine output at 100-150 ml/h (loop diuretics if renal or heart failure)
- 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
Hypophosphatemia definition
PO4 <2.6 mg/dL
Hypophosphatemia causes
Glucose loading Respiratory alkalosis Sepsis DKA Decreased absorption of phosphate
Hypophosphatemia clinical presentation
Usually asymptomatic, but may cause anemia, CHF exacerbation, weakness, shift of oxyghemoglobin curve to the left
Hypophosphatemia management
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
Hyperphosphatemia definition
POV >4.8 mg/dL
Hyperphosphatemia causes
Renal failure
Tumour necrosis
Hyperphosphatemia clinical presentation
usually asymptomatic
Hyperphosphatemia management
Sucralfate 1 g PO QID
Hemodialysis
Hypomagnesemia definition
Mg <1.5 mg/dl
Hypomagnesemia causes
medication: diuretics (Furosemide), aminoglycosides, cisplatin
diarrhea
diabetes
alcoholism
Hypomagnesemia clinical presentation
low Na, K, Ca or PO4
arrhythmia
seizure
Hypomagnesemia management
oral replacement: Magnesium oxide 400mg PO daily or Magnesium gluconate 500mg PO daily
IV replacement: Magnesium sulphate 1-2g over 1 hour infusion
Hypermagnesemia definition
> 2.5 mg/dL
Hypermagnesemia cause
Hemolysis
Renal failure
Hypermagnesemia clinical presentation
hyporeflexia (Mg = 4mg/dL) -> complete heart block (10mg/dL) -> cardiac arrest (13mg/dL)
Hypermagnesemia management
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
Indications for intubation
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)
Alternative to endotracheal intubation if patient is conscious
Nasotracheal intubation
Hypoxemia oxygenation intervention order
In order of increasing FiO2
Nasal prongs simple face mask non-breather masks CPAP/BiPAP mechanical ventilation
What should you do for someone not ventilating
Lack of ventilation requires bag-valve mask or assisted ventilation (CPAP, BiPAP) or mechanical ventilation
Differentiate the 4 classes of hemorrhagic shock
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
How to resuscitate the 4 classes of hemorrhagic shock
Crystalloid for class I and II Crystalloid + blood for class III and IV
What is an adequate IV fluid challenge
2L, where patient who is still hypotensive and tachycardic after challenge requires blood transfusion and investigation/management for ongoing bleeding
Procedure of giving blood transfusion
Start with 2 units of RBCs
Add plasma/platelets after giving 6 units of RBC
Role of vasopressor in resuscitation of trauma patients
None – may mask vitals
Resuscitation end points (ie return to normal perfusion)
- Restoration of normal vital signs
- Tissue perfusion (MAP 65 mm Hg plus; CVP 8-12 mm Hg when central access available)
- 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
- End-organ perfusion (normal mental status, urine output >0.5-1 cc/kg/h, warm skin with normal cap refill)
How to calculate MAP
[2 x diastolic + systolic] /3
GCS Score
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
AVPU score
Best response of patient awake spontaneously, responds to voice, responds to pain or unresponsive
What history should be taken in a trauma situation
SAMPLE Signs and symptoms Allergies Medication Past medical history Last meal Events related to injury
What is Cushing reflex
Seen in increased ICP
Hypertension, bradycardia, irregular respiratory rate
Contraindication to NG tube insertion
Suspected basal skull fracture
Why does metabolic alkalosis occur with hypovolemia
Pre-renal acute renal injury inhibits the kidney’s ability to excrete bicarb
