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Large animal medicine I > Critical Care Medicine > Flashcards

Critical Care Medicine Flashcards

1
Q

List the steps leading from disease to multi-organ failure.

A

Disease -> Sepsis -> Endotoxemia -> Systemic Inflammatory Response Syndrome -> Compensatory Autoimmune Response Syndrome -> Multi-organ Disfunction Syndrome -> Multi-organ failure

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2
Q

What is the most common cause of death for patients that are admitted to the ICU?

A

Multi-organ failure/dysfunction

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3
Q

Name two types of MODS/MOF.

A
  1. ) Acute respiratory distress syndrome (ARDS)

2. ) Disseminated intravascular coagulation (DIC)

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4
Q

List the criteria (2 minimum) required to diagnose SIRS (systemic inflammatory response syndrome)

A

Leukopenia, leukocytosis, hyper/hypothermia, tachycardia, tachypnea, sepsis

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5
Q

T/F: Gram negative bacteria are more commonly represented in endotoxemia.

A

True.

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6
Q

Describe the pathophysiology of endotoxemia.

A

Bacteria are killed during rapid prolifersation -> lysis. LPS activates cells (Lipid A is the responsible for toxic effect)

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7
Q

Name the 3 structural domains of LPS.

A

Polysaccharide O region (outer), Core acid polysaccharide (connecter), Lipid A region (inner)

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8
Q

How does the body defend against LPS and bacterial virulence factors?

A

Mucosal layer, physical barrier, lysozyme & enzyme secretions, circulating anti-endotoxin antibodies, macrophages

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9
Q

What are the five stages of endotoxemia?

A
  1. ) Endotoxins breach the physical barrier
  2. ) Endotoxins stimulate macrophages (chemical)
  3. ) Cytokine production. Leukocyte activity, procoagulation activity
  4. ) Compromised organ perfusion
  5. ) Recovery(?)
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10
Q

What is a sign you will see with initial endotoxemia?

A

Colic. (abdominal pain)

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11
Q

What are some things that can predispose the horse to endotoxemia?

A

Enteritis, colitis (potomac horse fever), sand colic, grain overload, drugs, pleuropneumonia, thoracotomy, choke, clostridium (skin), retained placenta (>2 hours), Equine Metabolic syndrome

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12
Q

How does equine metabolic syndrome lead to endotoxemia?

A

EMS horses have more cytokine factors, leads to increased and prolonged inflammation from exposure to LPS

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13
Q

Describe how LPS interacts with the host immune system.

A

The host cell PRR’s interact with LPS (PAMP) and produce pro/anti-inflammatory factors. LPS leads to MyD88 -> pro-inflammatory

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14
Q

At what stage of endotoxemia does endothelial damage and hypercoagulation occur?

A

Stage 3. (of 5)

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15
Q

Describe how Stage 4 endotoxemia leads to multi-organ failure.

A

Loss of perfusion, vasodilation and vascular leakage, coagulation, and overall hypotension to the organs leads to dysfunction -> failure

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16
Q

How does the Recovery stage (5) work?

A

LPS induces IL10 which inhibits pro-inflammatory cytokines.

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17
Q

Concerning experimental endotoxemia, what clinical signs will you see early on (90 minutes)?

A

Tachypnea, pale MM, fever, restlessness

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18
Q

Concerning experimental endotoxemia, what clinical signs will you see at 2 hours?

A

Peak tachypnea, congested MM, increased CRT, decreased GIT sounds

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19
Q

Concerning experimental endotoxemia, what clinical signs will you see at 4-6 hours? (secondary phase)

A

Tachycardia, fever, circulatory failure, coagulopathy, dehydration! (sunken eye, skin tenting)

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20
Q

Why would a dehydrated horse still produce urine?

A

Strong regulatory renal function causes the renal artery to vasodilate and work.

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21
Q

Concerning experimental endotoxemia, what clinical signs will you see in its later stages?

A

Decreased rectal temperature, oli/anuria, rapid weak pulses, muscle tremors, hemodysfunction

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22
Q

Concerning experimental endotoxemia, what clinical signs will you see after 24 hours?

A

ventral edema, laminitis

those that do not show signs of laminitis are more worrisome

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23
Q

T/F: Horses have less sensitivity to LPS compared to other species

A

False. Higher sensitivities!

Flagellin typically activates monocytes in animals, but for horses its NEUTROPHILS

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24
Q

List some symptoms seen with the hyperdynamic state of clinical endotoxemia.

A

white mucous membranes, normal CRT, strong pulses, tachypnea, fever/hyperthermia

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25
Q

List some symptoms seen with the hypodynamic state of clinical endotoxemia.

A

dark mucous membranes, prolonged CRT, weak pulses, tachypnea, cold extremeties, normal/hypothermic

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26
Q

What is a ‘toxic line’?

A

area on the mucous membranes (oral) that signifies endotoxemia. better to look for petechia

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27
Q

What CBC results will you see on a horse with endotoxemia?

A

leukopenia, neutropenia with a left shift

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28
Q

List some diagnostic factors you can measure through blood work.

A

Glucose, lactate (measures severity), platelets, fibrinogen

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29
Q

What is the limulus ameobocyte lysate assay?

A

It is the direct measurement of circulating endotoxins. Typically more for research purposes.

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30
Q

List the three types of limulus ameobocyte lysate assays.

A
  1. ) Gel Clot Assay (clots with presence of endotoxins)
  2. ) Turbidi-metric testing (use of measuring light beams)
  3. ) Chromogenic limulus amebocyte lysate
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31
Q

Why is it important to recognize endotoxemia early on? (think common sense)

A

early treatment to prevent multiorgan dysfunction and laminitis

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32
Q

Why is preventing laminitis so important when working with potential endotoxemia?

A

Studies show preventing laminitis provides a better prognosis.

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33
Q

What are the goals of treating endotoxemia?

A

Support circulatory system, removal the causes, neutralize the endotoxin and inhibit its inflammation, prevent laminitis

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34
Q

What are some treatment methods for endotoxemia?

A

IV fluids (preferable polyionic solution - LRS or normosol), treating the cause, certain medications

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35
Q

How do PAMP antibodies fight against endotoxemia?

A

the antibodies bind and neutralize LPS. shown to decrease mortality rate

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36
Q

What is a potential concern with anti-microbial therapy against endotoxemia?

A

Rapid death of the bacteria and exacerbate the endotoxemia. (not super significant)

37
Q

What is the name of the effective neutralizing antibiotic that directly interferes with lipid A?

A

Polymixin B. Decreases LPS activity and inflammatory response

38
Q

What is a potential side effect of polymixin B?

A

Renal toxicity.

39
Q

What NSAID is recommended for use in endotoxemia?

A

Flunixin meglumin. Works very well with the inflammation. Watch out for nephrotoxicity.

40
Q

T/F: glucocorticoid steroids are an effective and safe way of treating endotoxemia

A

False. very controversial

41
Q

How can DMSO treat endotoxemia?

A

Decreases cytokine expression and macrophage inflammatory responses. Also decreases fever

42
Q

T/F: Ketamine CRI is recommended in use of treating endotoxemia.

A

True! Works well against LPS-induced cytokine formation and reduces inflammation

43
Q

How does Lidocaine CRI work against endotoxemia?

A

Works against inflammation in the GIT, which leads to better motility.

44
Q

The vast collection of medications for endotoxemia are available, but not fully definitive. What is the best treatment for endotoxemia?

A

Aggressive supportive care. (fluids)

45
Q

T/F: vaccination against endotoxemia is extremely effective.

A

False

46
Q

What is DIC?

A

The activation of the coagulation system which leads to the inappropriate level of coagulation and secondary hemorrhage

47
Q

What are some main causes of equine DIC?

A

Sepsis, endotoxemia, SIRS, immune-mediated diseases, neoplasia

48
Q

What factor in the coagulation cascade is lower to equines that may predispose them to DIC?

A

Antithrombin III

49
Q

What are four clinical pathologic abnormalities seen with DIC?

A

Procoagulation, fibrinolysis, consumption of inhibitors, and organ damage

50
Q

What are some obvious signs of DIC?

A

There aren’t really any until it is terminal

51
Q

What is one way to identify subclinical DIC?

A

These signs may be compatible with SIRS/MODS

52
Q

What are some clinical signs of DIC with horse with SIRS?

A

Petechia, prolonged bleeding, spontaneous bleeding, rapid death

53
Q

What is the most common complication with horses that have DIC after venipuncture?

A

Jugular thrombophlebitis.

54
Q

What are some detection methods for coagulation FACTOR consumption?

A

PT (prolonged prothrombin time), aPTT (activated partial thromboplastin)

55
Q

What are some tests that detect coagulation factor INHIBITOR consumption?

A

Antithrombin

56
Q

What can you measure that tells you how much fibrin has been formed, especially when suspecting DIC?

A

D-dimers.

57
Q

What are the goals in treating DIC?

A

Control the underlying disease, anti-microbial therapy

58
Q

T/F: the use of hetastarch is controversial in horses when treating DIC.

A

True. can potentially cause excessive bleeding

59
Q

T/F: Heparin is a good treatment option for DIC in its hypercoagulable phase

A

True.

60
Q

How does low molecular weight heparin (LMWH) work?

A

It reduces excessive fibrin deposition and coagulation consumption

61
Q

How would you treat DIC in its hypocoagulable phase?

A

Plasma transfusion to replace platelets and factors that have been consumed.

62
Q

What does Yunnan Baiyao do?

A

Treats hemorrhages and wounds and has an anti-inflammatory/immunosuppressive function

63
Q

What is a major consequence and cause of death in animals with DIC?

A

Hypercoagulation and fibrin thrombi deposited in the capillaries -> MODS/MOF

64
Q

List some meds that are contraindicated in DIC.

A

Antifibrinolytics (enhances hypercoagulation), hypertonic saline solution (dilution of factors), hetastarch

65
Q

What bone is directly attached to the lamina?

A

Distal phalange/ coffin bone

66
Q

Define laminitis.

A

Inflammation of the lamellae of the inner hoof capsule. Painful

67
Q

What are some common organ systems that can have issues along side laminitis?

A

GI, lungs, repro, endocrine, musculoskeletal, skin, immune, renal

68
Q

What are some factors that may cause laminitis?

A

endotoxemia endocrine diseases, trauma, drugs, toxins

69
Q

How does SIRS cause laminitis?

A

The leukocytes during the systemic inflammation infiltrate the epithelial layer and cause stress (cytokines, ROs, etc)

70
Q

T/F: Vascular hypothesis of laminitis is the belief that there are factors pertaining to the vasculature of the digits that lead to poor perfusion and thus ischemia, causing swelling and inflammation as a response.

A

True.

71
Q

T/F: Hypoinsulinemia can cause laminitis in horses.

A

False. Hyperinsulinemia

72
Q

If you see a foal with laminitis, what is the most likely cause?

A

Endotoxemia. Salmonellosis.

73
Q

How can excessive weight loading cause laminitis?

A

Tearing of the sensitive tissues, induces vasospasms, fatigue and vasocompression

74
Q

T/F: Hoof capsule injuries are difficult to regenerate if damaged.

A

True.

75
Q

How will a horse stand if it has laminitis in all four feet?

A

With its neck pressed back and head up

76
Q

How will a horse stand if it has laminitis in only the front feet?

A

With its neck dropped and head low

77
Q

What are the four Obel grades of laminitis?

A

Grade I: shifts weight, but freely moves

Grade II: lameness more obvious, but can still bear some weight and lift other foot

Grade III: Cannot bear as much weight and give contralateral foot

Grade IV: more severe, cannot move, recumbent.

78
Q

How thick should the HLZ be when normal? With lamintis?

A

16-18 mm normal. 22 with laminitis.

79
Q

At what phase of laminitis is it best to prevent it?

A

Developmental phase

80
Q

Whats the best way to prevent laminitis in its developmental phase?

A

Treat the primary cause. Cryotherapy works too!

81
Q

What are some medications for acute laminitis?

A

NSAIDS (flunixin meglumine, phenylbutazone)

Butorphanol, Lidocaine CRI (very good), DMSO

82
Q

What is a potentially issue with wooden shoes?

A

Difficult to wean the horse off of it.

83
Q

What factors determine the prognosis of laminitis?

A

amount of lamellar damage, hoof conformation, duration, coronary band damage, vascularity

84
Q

What is a difference between chronic compensated and chronic uncompensated laminitis?

A

The coffin bone is displaced, but is stabilized to some degree in the compensated form. Uncompensated is not and is extremely painful

85
Q

What can a venogram do in regards to laminitis?

A

It can assess the level of vascular damage.

86
Q

Where are three locations in which there can be deficits in perfusion?

A

Dorsal lamina, circumflex vessels, coronary plexus

87
Q

What are some surgical forms of treatment for laminitis?

A

DDF tenotomy, coffin joint subluxation

88
Q

List some coronary band pathologies.

A

Shear lesions, partial hoof wall resection, infection/osteomyelitis, marginal rim fracture, flexor tendon contracture

Large animal medicine I (6 decks)

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