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Surgery Clerkship > Surgical Complications > Flashcards

Surgical Complications Flashcards

1
Q

What’s in the differential for bleeding in the post-op setting?

A

Surgical bleeding: bleed from artery/vein in surgery
Meds
Inherited coag d/o
Liver disease: reduced clotting factor production
Renal failure: uremia impairs platelet function
DIC

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2
Q

What is the bloody vicious cycle or the lethal triad of death?

A
  • Trauma
  • Large volume of room temp IV fluids
  • Long operations
    (More common in those with sign. bleeding)
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3
Q

What is the differential for prolonged PTT?

A 
Acquired FVIII inhibitors
Antiphospholipid syndrome
Hemophilia A / B
Heparin
Von Willebrand disease
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4
Q

Why do we ask about history of bleeding after minor trauma/procedures?

A

Predisposition to bleeding risk!

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5
Q

Why do we ask about family history of bleeding?

A

Suggests inherited bleeding disorder

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6
Q

What medical conditions are risk factors for bleeding?

A 
Liver disease (clotting factors deficient)
Kidney disease (uremia inhibits platelets)
Malabsorption syndrome (vit K def)
Cardiac dz due to the meds
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7
Q

What is difference between primary and secondary hemostasis disorders?

A

Primary: platelets
Secondary: factor abnormalities

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8
Q

What is coagulopathy?

A

Impairment of body’s ability to clot blood

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9
Q

What is a medical vs. surgical post-op beed?

A

Surgical: bleeding that can be corrected w/ surgery (bleeding from focal artery/vein that was inadequately ligated or sutured during initial surgery)
Medical: diffuse bleeding caused by underlying coagulopathy

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10
Q

How does renal failure cause coagulopathy?

A

Uremic toxins in blood –> platelet dysfunction

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11
Q

How do we manage coagulopathy in setting of renal failure?

A

Desmopressin (acutely) and/or

HD (definitively)

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12
Q

How does liver disease cause coagulopathy?

A

Synthetic liver function decreased and thrombocytopenia: prolonged PT and INR

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13
Q

Why do surgical bleeds occur?

A

Inadequate hemostasis

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14
Q

What are risk factors for coagulopathy?

A 
Copious IV fluids/transfusions
Hypothermia
Metabolic acidosis
Liver/Kidney dsiease
DIC
Fam history of bleeding
Anticoagulants
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15
Q

What to think: coagulopathy in patient who recently started heparin?

A

HIT: platelets drop > 50% because of Ab formed by heparin + platelet factor 4 that destroy platelets

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16
Q

What’s the most common cause of thrombocytopenia?

A

Alcohol use

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17
Q

What are the 3 main causes to think about for DIC?

A

Delivery (pregnancy): tissue thromboplastin in amniotic fluid activates coag cascade
Infection: sepsis causes endothelial cells to make tissue factor
Cancer: Auer rods in AML activate coagulation cascade

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18
Q

What is mechanism of DIC?

A

Clotting cascade activation –> deficiency of factors –> abnormal bleeding

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19
Q

What is the primary treatment of DIC?

A

Treat underlying cause

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20
Q

What is physiological fibrinolysis?

A

Generation of fibrin: occurs when plasmin binds to it: breaks down clots to limit extent of clot formation

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21
Q

What can abnormal activation of fibrinolytic pathway cause?

A

Bleeding and excess plasmin which consumes clotting factors –> more bleeding

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22
Q

What is the most important diagnostic modality for coagulopathy?

A

Clinical history

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23
Q

What is the treatment of hepatic coagulopathy?

A

FFP

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24
Q

What is the reversal for heparin? warfarin?

A

Heparin: Protamine sulfate
Warfarin: FFP and Vit K, or prothrombin complex concentrates

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25
Q

For most elective procedures, what level of platelets is sufficient?

A

> 50,000

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26
Q

At what point should re-exploration be considered for a patient who is bleeding post-op?

A

Only in surgical bleed: medical bleed must be deemed unlikely and patient continues to actively bleed

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27
Q

What is the leading cause of transfusion-related fatalities?

A

Transfusion-Related acute lung injury (TRALI): donor Ab attack recipient’s WBC - aggregates in lungs and releases inflammatory mediators

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28
Q

How do we treat TRALI?

A

IV fluids
Vasopressors
Respiratory support

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29
Q

How long before surgery should we stop aspirin? Clopidogrel?

A

Aspirin: 4 days
Clopidogrel: 7-10days

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30
Q

How long after warfarin is stopped will INR fall below 2.0? To normalize?

A

< 2.0: 2-3 days

Normalize: 4-6 days

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31
Q

What’s the differential diagnosis for AKI in the post-op setting (categories)?

A
  1. Prerenal
  2. Intrinsic
  3. postrenal
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32
Q

What’s the pre renal cause of AKI post-op?

A

Hypovolemia or decreased CO causing hypo perfusion of kidney

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33
Q

What’s the intrinsic renal cause of AKI post-op?

A

ATN or interstitial nephritis: prolonged ischemia of the kidney or toxins leading to parenchymal injury

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34
Q

What’s the postrenal renal cause of AKI post-op?

A

Obstruction: BPH, prostate cancer, nephrolithiasis: all cause increased nephron tubular pressure

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35
Q

What’s the most common cause of decreased urine output post-op?

A

Hypovolemia/dehydration decreasing perfusion to kidney

36
Q

What thins do we look for on the operative and anesthetic record in decreased urine output?

A
  • Events that could cause!
  • Blood loss
  • Complications
  • Anticoagulants
37
Q

What is the most common presentation of AKI?

A

Prerenal azotemia: rise in BUN and creatinine

38
Q

What is the earliest sign of AKI?

A

oliguria

39
Q

What are the standards of oliguria vs. anuria?

A

Oliguria: adult: 0.5-1.0 mL/kg/hour
Anuria: <50-100 mL per 24 hours

40
Q

What are the most common nephrotoxic meds?

A 
Contrast
Aminoglycosides
Amphoterocin
Cispatin
Cyclosporine
NSAIDs
41
Q

Who is at greatest risk for IV-contrast induced AKI?

A

Patients with pre-existing renal damage!

42
Q

What can help to prevent contrast-induced renal failure?

A

N-acetylcysteine
Bicarbonate
Normal saline hydration

43
Q

What rise in creatinine defines contrast-induced AKI?

A

Increase of creatinine of 0.5mL/dl within 48-72 hours

44
Q

What are the hormones primarily responsible for post-op oliguria?

A

ADH

Aldosterone

45
Q

What else can cause increased BUN/Cr ratio?

A

UGI bleed: high protein absorption
Increased urea production (steroid therapy)
Low muscle mass (low serum creatinine)

46
Q

After surgery, what duration of oliguria warrants investigation?

A

24 hours

47
Q

What’s the best initial test when suspecting AKI?

A

BUN and Cr: BUN/Cr > 20:1 with history of hypo- perfusion

48
Q

What other tests, besides BUN and Cr, can help workup AKI?

A

UA
Urine Na
FENa
Urine osmolality

49
Q

What imaging is useful in the work-up of oliguria?

A
  • US to look for obstruction: bladder, kidneys, ureters

- Doppler US for renal perfusion

50
Q

When encountering low urine output, what 3 simple things must be done first?

A
  1. Rule out obstructed Foley
  2. Stop nephrotoxic drugs
  3. Do a fluid challenge
51
Q

What is a fluid challenge?

A

Give an oliguric patient a bolus of NS (0.5-1L) over 30 minutes to see if they increase urine output

52
Q

What should be done for an oliguric patient if they’re suspected of having a post-renal obstruction?

A

Give a Foley catheter to relieve it

53
Q

What are the indications for urgent/emergent dialysis?

A 
AEIOU
Acidosis
Electrolyte abnormalities (Hyperkalemia)
Intoxication (ethylene glycol)
Overload (fluid)
Ureimia
54
Q

What’s in the differential for post-op SOB?

A 
Pneumonia
PE
MI
Pneumothorax
Cardiogenic/non pulmonary edema
Anxiety
Bleeding
55
Q

What is Virchow’s triad?

A

Stasis
Endothelial injury
Hypercoaguable state

56
Q

What is the Wells’ score cutoff for high likelihood of PE?

A

> 4

57
Q

Which leg is more often affected by DVT and why?

A

Left: L iliac vein is often compressed by the R iliac artery (May Thurner syndrome)

58
Q

What signs are associated with PE?

A

Sudden onset dyspnea, pleuritic chest pain, and/or tachycardia

59
Q

What are the 5 classic causes of post-op fever?

A 
Wind: Atelectasis POD1-2
Water: UTI: POD3+
Wound: infection POD5+
Walking: DVT/thrombophlebitis: POD 7-10
Wonder drugs: drug fever anytime
60
Q

What are the most common acquired causes of hypercoaguability?

A 
Advanced age
Pregnancy
Malignancy
OCPs
Hormone replacement
Smoking
Obesity
Nephrotic syndrome
HIT
61
Q

What can be the cause of cardiogenic pulmonary edema on post-op day 3?

A

Third spacing: large volume of IV fluids given during surgery return back to the vasculature and poor heart function places you at risk to overwhelm the hert

62
Q

What are the 3 routes by which a patient develops post-op pneumonia?

A

Inhalation
Aspiration
Hematogenous spread

63
Q

What’s the differential of a wide A-a. gradient in the post-op setting?

A

Atelectasis
pneumonia
PE

64
Q

What’s the first step in the work-up of a patient suspected of having a PE?

A

Calculate Wells Score

65
Q

If there is a high suspicion of DVT, what it is the first step in workup?

A
  1. Heparin immediately to stop clot propagation

2. CT angiogram

66
Q

If there is a low suspicion of DVT, what it is the first step in workup?

A

D-dimer assay because of negative predictive value

- If elevated: CT angiogram

67
Q

In PE patient, what are most common findings on ABG?

A

ABG: Acute respiratory. alkalosis, hypoxemia, increased A-a gradient

68
Q

In PE patient, what are most common findings on CXR?

A

Normal

69
Q

In PE patient, what are most common findings on ECG?

A

Sinus tach

70
Q

What other labs should be sent in suspected PE?

A

D-dimer
BNP
Troponin labs

71
Q

If CT angiogram is non-diagnostic in suspected PE, what is the next step?

A

V/Q scan

72
Q

Why has V/Q scan fallen out of favor for diagnosing PE?

A

Because a significant percentage of patients with low probability on V/Q scan end up actually having a PE

73
Q

If a patient is critical ill and cannot be transported for imaging, what bedside options are available for indirect diagnosis of PE?

A

Echocardiogram can show R heart strain, or doppler US can show venous thrombosis

74
Q

What is a low risk PE?

A

No evidence of RV dysfunction or myocardial necrosis

75
Q

What is a submassive PE?

A

Evidence of RV dysfunction on echo, or myocardial necrosis (based on NBP or elevated troponin)

76
Q

What is a massive PE?

A

Evidence of RV dysfunction on echo, or myocardial necrosis (based on NBP or elevated troponin)
PLUS sustained hypotension

77
Q

What is the initial anticoagulant management of PE?

A

Heparin or LMWH

78
Q

If a patient with suspected PE has contraindication to anticoagulation, what to do?

A

Place IVC filter

79
Q

What are the treatment options for PE after initial anticoagulation?

A
  1. Heparin alone
  2. tPA
  3. Endovascular clot aspiration
  4. open pulmonary embolectomy
80
Q

When is tPA used for PE?

A

Massive PE, should be considered in submissive PE

81
Q

How do we treat submassive PE?

A

Heparin/LMWH and consider tpa

82
Q

How do we treat massive PE?

A

tPA or pulmonary embolectomy

83
Q

What is the recommendation for long-term anticoagulation after first time VTE?

A
  1. Heparin/LMWH for first 5 days
  2. Start warfarin day 2 to bridge
    * * Anticoagulate for at least 3 months after VTE, at least 6 months if recurrent or unprovoked
84
Q

Which anticoagulant to use in patients with VTE and malignancy?

A

LMWH

85
Q

Which anticoagulant to use in patients with VTE and history of HIT?

A

Direct thrombin inhibitors

Surgery Clerkship (16 decks)

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