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accs > kettering section c: general critical care > Flashcards

kettering section c: general critical care Flashcards

1
Q

identify the quantitative markers of acute hypoxemic respiratory failure

A
  • PaO2 <= 50-60mmHg on room air
  • SpO2 < 93% on room air
  • PaO2/FiO2 ratio < 300
  • A-aDO2 > 200 mmHg
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2
Q

Name five hypoxemic mechanisms.

A
  • V/Q mismatch
  • Decreased diffusion of oxygen across the alveolar-capillary membrane
  • Alveolar hypoventilation (hypercapnia)
  • High altitude with low inspired PO2
  • Shunt / refractory hypoxemia / venous admixture
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3
Q

Identify quantitative markers of hypercapnic respiratory failure.

A
  • PaCO2 >= 50 mmHg
  • FVC < 10 mL/kg
  • NIF less negative than -20 cmH2O
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4
Q

Name the ATS/ERS criteria for ARDS.

A
  • P/F ratio < 200
  • PCWP < 18 mmHg
  • Diffuse bilateral infiltrates
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5
Q

Name the phases of ARDS

A
  • Exudative
  • Proliferative
  • Fibrotic
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6
Q

Characterize the exudative phase of ARDS.

A

Starts within 12-36 hours of insult to lung
Lasts 1 - 7 days
Features alveolar and leukocytic inflammation with hyaline membranes from diffuse alveolar damage–more prevalent in gravity-dependent portions of the lungs
Features hypoxemia, tachypnea, and progressive dyspnea
Features increase in physiologic deadspace that leads to hypercarbia
Appears on CXR as bilateral, diffuse alveolar and interstitial opacities

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7
Q

Characterize the proliferative phase of ARDS.

A

Lasts 7-21 days
Features persistent dyspnea and hypoxemia
May develop in some patients progressive lung injury and fibrosis

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8
Q

Characterize the fibrotic phase of ARDS.

A

Leads to recovery for most patients in 3 - 4 weeks
Means for some patients progressive fibrosis with prolonged mechanical ventilation and/or supplemental oxygen therapy

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9
Q

Name a bunch of risk factors for acute coronary syndrome.

A

Family history of MI
Hypertension
History of smoking
Hyperlipidemia
Increasing age
Post-menopausal state
Obesity
DM
Other vascular diseases
Sedentary lifestyle
Cocaine/amphetamine use

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10
Q

What information do you need to gather to form a diagnosis of ACS?

A

History
Clinical assessment
Electrocardiogram (12-lead ECG)
Serum biomarkers

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11
Q

Name clinical presentations of ACS.

A

SOB
CP
Fine basilar crackles on auscultation
Diaphoresis
Nausea & vomiting

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12
Q

What’s the leading cause of death from ACS?

A

Cardiogenic shock.

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13
Q

For patients who don’t tolerate aspirin for anti-platelet aggregation therapy, what should be offered to them?

A

Clopidogrel
Ticlopidine

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14
Q

Name the anti-ischemic meds.

A

Nitroglycerin
Morphine
Beta blockers
Diltiazem

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15
Q

What class of medication is Diltiazem?

A

Calcium-channel blocker

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16
Q

Name a calcium-channel blocker?

A

Diltiazem.

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17
Q

Clinical presentation of NSTEMI.

A
  • Angina at rest, new-onset angina, or increasing angina
  • Prior history of CAD
  • S/T segment depression on serial EKGs
  • Elevated biochemical markers (troponin, CK-MB)
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18
Q

How to manage NSTEMI.

A

–Admit to unit with cardiac monitoring
–Provide oxygen for anyone with dyspnea, SpO2 < 90% on RA, evidence of heart failure, evidence of shock
–Correct any precipitating factors, such as fever, anemia, anxiety, hypertension
–Control pain with analgesia–nitroglycerin, morphine
–Supply anti-ischemic medications
–Provide medication to combat platelet aggregation/thrombosis
–Provide anticoagulation agents
–Consider reperfusion procedures

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19
Q

Describe clinical presentation of STEMI.

A

Prolonged chest pain
S4 heart sound
Bibasilar crackles
Serial EKG with S/T segment elevation
Elevated biochemical markers–troponin, CK-MB

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20
Q

How to manage STEMI.

A

Supply blood flow to affected area
Oxygen
Aspirin/Clopidogrel
Nitroglycerin / morphine
Heparin
Beta-blocker
Invasive reperfusion in the cath lab

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21
Q

Okay–slog through the steps for the apnea test.

A

Hyperoxygenate patient to reach PaO2 > 200 mmHg
Disconnect patient from ventilator while monitoring SpO2
Administer 100% oxygen
Observe closely for chest or abdominal movements which produce an adequate Vt.
–** presence of respiratory movements indicates a negative apnea test
–absence of respiratory movements indicates a positive test and supports a diagnosis of brain death
Obtain an ABG after 8 minutes and reconnect patient to ventilator

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22
Q

Criteria for diagnosis of brain death

A

–Total cessation of cerebral function while somatic function is maintained by artificial means and the heart continues to beat
–Lack of response to all forms of stimulation (showing widespread cortical destruction)
–Absence of brainstem reflexes (showing global brainstem damage)
–Apnea (showing destruction of medulla)
–Exclusion of hypothermia and drug toxicity (prior to brain death diagnosis)

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23
Q

What definitive test confirms diagnosis of brain death?

A

Cerebral perfusion scan (cerebral angiogram)

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24
Q

Formula for cerebral perfusion pressure

A

MAP - ICP

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25
Q

Cerebral perfusion pressure normal values

A

60 - 100 mmHg

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26
Q

Critical values cerebral perfusion pressure

A

20 - 40 mmHg

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27
Q

Why would we place an ICP monitor?

A

–To detect life-threatening elevations of ICP
–To assess effectiveness of therapy
–To drain CSF to therapeutic effect

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28
Q

What are contraindications to placing an ICP monitor?

A

–Coagulopathy (low platelets, APTT 2x normal)
–Immunosuppressive therapy (particularly steroids)

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29
Q

Name six non-surgical strategies to reduce and/or maintain low ICP.

A

Maintain low jugular venous pressure.
Provide sedation and analgesia.
Remove fluid from brain with osmotic agents.
Hyperventilate.
Avoid hypoventilation and hypoxemia.
Use normal saline as primary maintenance fluid.

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30
Q

How does one maintain low jugular venous pressure to keep ICP from climbing?

A

Position patient carefully to avoid threats to venous drainage–
* Avoid neck flexion
* Avoid head turning
* Ensure trach tube ties are not too tight
Minimize increase in central venous pressure–
* Keep head of bed elevated to 30 degrees
* Minimize straining, retching, coughing
* Minimize PEEP

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31
Q

What osmotic fluids can help reduce fluid from the brain?

A

Mannitol
Hypertonic saline

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32
Q

Kettering on hyperventilation for reducing ICP

A

–PaCO2 of 25 - 30 mmHg
–Works only temporarily
–Results temporarily in vasoconstriction
–May be effective for acute elevations in ICP
–Many not be considered a standard of care

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33
Q

After seizure activity, return to consciousness is delayed. What conditions should be on differential diagnosis?

A

Stroke
Subarachnoid hemorrhage
Subdural hematoma
Tumor
Underlying metabolic disorder (e.g., hypoglycemia, toxin ingestion, electrolyte disturbance)

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34
Q

Kettering on pharmacological treatment of progressive ischemic stroke

A

tpa
Aspirin

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35
Q

Which tests confirm an SAH?

A

CT scan
Lumbar puncture

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36
Q

What’s the window for vasospasm following SAH?

A

3-5 days.

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37
Q

In cardiogenic shock, low cardiac output could be caused by what two factors?

A

• Intravascular volume depletion (e.g. hemorrhage)
• Cardiac dysfunction

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38
Q

Types of shock—four

A

Cardiogenic
Hypovolemic
Obstructive
Distributive

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39
Q

Mechanisms of shock—three

A

Failure of pump
Failure of vascular tone
Failure of fluid volume

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40
Q

Divide the shocks into two varieties.

A

Low cardiac output (cardiogenic, hypovolemic, obstructive)
High cardiac output (distributive)

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41
Q

Name that shock:

High cardiac output
Decreased MAP
Decreased SVR
Normal to low CVP
Normal to low PCWP
Increase pulse pressure

A

Distributive shock

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42
Q

Name six conditions that could lease to distributive shock.

A
  • Sepsis
  • Adrenal insufficiency
  • Hyperthyroidism
  • Anaphylaxis
  • Hepatic failure
  • Neurologic dysfunction—post-anesthesia, spinal cord injury
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43
Q

What is the mortality rate of acute renal failure?

A

60%!

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44
Q

Three urine output markers for oliguria

A

< 400 mL/day (UTD)
< 17-40 mL/hr
< 0.5 mL/kg/hr (UTD)

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45
Q

Name 7 potential causes of oliguric renal failure.

A
  1. Low cardiac output from hypovolemia
  2. Mechanical ventilation
  3. Aortic stenosis
  4. End-stage cardiomyopathy
  5. Drug therapy (ACE inhibitors)
  6. Renal injury
  7. Post-renal obstruction
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46
Q

In cases of traumatic myoglobinuric renal failure, what should you see?

A

CPK >5000 IU/L
Brown urine

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47
Q

Causes of myoglobinuric renal failure—K’s bumper sticker list

A

Trauma
Infection
Immobility
Drugs
Hypophosphatemia
Excessive exercise

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48
Q

What values should be watched closely in cases of myoglobinuric renal failure?

A

Potassium
Phosphate (PO4-3)

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49
Q

Evaluate oliguria with these six pointers

A

CVP may overestimate cardiac filling volume in critically ill patients.

For patients on mechanical ventilation, CVP levels as high as 10 to 20 mmHg can still indicate hypovolemia.

Respiratory variation in blood pressure (pulsus paradoxus) May be evidence of hypovolemia.

Decreases in blood pressure shortly after lung inflation can be used as evidence of decreased preload and inadequate cardiac filling.

Central venous saturation (SvO2) of 25-30% would indicate low cardiac output.

In patients with systemic sepsis, SvO2 < 70% is considered abnormal.

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50
Q

What conditions call for aborting an apnea test for brain death evaluation?

A

–Systolic BP slides below 90 mmHg.
–Significant oxygen desaturation occurs.
–Cardiac arrhythmias appear.
Obtain ABG immediately.
Evaluate PaCO2:
–PaCO2 > 60 mmHg or 20 mmHg above baseline supports a positive test for brain death
–PaCO2 <= 60 mmHg shows inconclusive results

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51
Q

Name pre-requisites for apnea brain death evaluation.

A

–Core body temperature >= 36.5degreesC
–Systolic BP > 90 mmHg
–Normal PaCO2 on mechanical ventilation

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52
Q

Six keys to management of oliguria

A
  • Identify and correct volume deficits
  • Discontinue any drugs that may cause oliguria
  • Fluid challenge, especially in patients with reduced preload (0.5-1L crystalloid; 300-500mL colloid for patients with sepsis)
  • Avoid low dose dopamine (dopamine makes patients pee–even when they shouldn’t–EMCRIT 138)
  • Diuretics (furosemide) via continuous IV infusion (intermittent doses are less effective)
  • Hemofiltration may be indicated for patients with high BUN, serum creatinine, and positive fluid balance
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53
Q

Define anorexia

A

“Lack of desire to eat despite physiologic stimuli that normally produce hunger” (UP)

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54
Q

What s/s are associated with anorexia?

A

Associated with nausea, abdominal pain, diarrhea

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55
Q

What is vomiting?

A

Forceful emptying of the stomach and intestinal contents through the mouth.

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56
Q

What may stimulate vomiting?

A

Severe pain
Distension of the stomach or duodenum
Trauma
Ipecac or copper salts in duodenum

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57
Q

What is retching?

A

Stomach and duodenum contract
but upper esophageal sphincter remains closed
material is maintained in esophagus

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58
Q

What is projectile vomiting?

A

Vomiting not preceded by nausea or retching

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59
Q

What is constipation?

A

Difficult or infrequent defecation
or
decrease in the number of bowel movements
or
hard stools

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60
Q

What may cause constipation?

A

Enlarged or dilated colon
Abdominal muscle weakness
Low-residue diet
Emotional depression
Medications such as opiates, anticholinergics, antacids

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61
Q

What is diarrhea?

A

Increase in the frequency of defecation and the fluidity and volume of feces

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62
Q

Name three types of diarrhea

A

Osmotic diarrhea
Secretory diarrhea
Motility diarrhea

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63
Q

What is osmotic diarrhea?

A

Diarrhea arising from a nonabsorbable substance in the intestine that draws excess water into the intestine and increases stool weight and volume (producing large-volume diarrhea). (UP 7th)

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64
Q

What is secretory diarrhea?

A

Large-volume diarrhea resulting from excessive mucosal secretion of fluids and electrolytes. (UP 7th)

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65
Q

What is motility diarrhea?

A

Diarrhea arising–roughly–from conditions where shortened gut or excessive motility decrease digestion transit time and the opportunity for fluid absorption. (UP 7th)

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66
Q

What is upper GI bleeding?

A

Bleeding in the esophagus, stomach, or duodenum

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67
Q

What is the most common type of upper GI bleed?

A

Bleeding ulcers

68
Q

What is lower GI bleeding differential?

A

Polyps
Inflammatory disease
Cancer
Hemorrhoids

69
Q

Name the clinical manifestations of gastrointestinal disorders

A

Abdominal pain
Vomiting
Diarrhea
Constipation
Anorexia
Gastrointestinal bleeding
Ileus

70
Q

Name the disorders of GI motility

A

Dysphagia
GERD
Hiatal hernia
Pyloric obstruction
Intestinal obstruction

71
Q

How is dysphagia evaluated?

A

Barium swallow
Esophageal endoscopy

72
Q

How are symptoms of dysphagia managed?

A

Eating slowly
Eating small meals
Taking fluid with meals
Sleeping with the head elevated

73
Q

What is GERD?

A

Reflux of gastric contents (chyme) from stomach to the esophagus

74
Q

How is GERD evaluated?

A

Esophageal endoscopy
Barium swallow
Ambulatory pH monitoring

75
Q

How to relieve symptoms of GERD?

A

antacids
elevation of the head of the bed
weight reduction
smoking cessation

76
Q

Medication classes for GERD

A

Proton pump inhibitors
H2 receptor antagonists
Prokinetic agents.

77
Q

Name the proton pump inhibitors

A

Omeprazole (Prilosec)
Lansoprazole (Prevacid)
Esomeprazole (Nexium)

78
Q

Name the H2 receptor antagonists

A

Cimetidine (Tagamet)
Ranitidine (Zantac)
Famotidine (Pepcid)
Nizatidine (Tazac)

79
Q

Name the prokinetic agents for GERD

A

Benzamide
Cisapride
Domperidone
Erythromycin

80
Q

What is a hiatal hernia?

A

Protrusion of the upper part of the stomach through the diaphragm and into the thoracic cavity.

81
Q

What factors contribute to formation of hiatal hernia?

A

–congenitally short esophagus
–trauma
–weakening of the diaphragmatic muscles at the gastroesophageal junction

82
Q

How do you evaluate hiatal hernia?

A

Barium swallow
Endoscopy

83
Q

How do you treat hiatal hernia?

A

Usually conservatively–
* eat small, frequent meals
* avoid recumbent position after eating

84
Q

What is pyloric obstruction?

A

Narrowing or blocking of the opening between the stomach and the duodenum (UP)

85
Q

Can one be born with pyloric obstruction?

A

yes–can be congenital or acquired (UP)

86
Q

What leads to acquired pyloric obstruction?

A

–peptic ulcer disease
–carcinoma near the pylorus (UP)

87
Q

What are the clinical manifestations of pyloric obstruction?

A
  • epigastric fullness after eating, later in day
  • nausea
  • epigastric pain
  • severe obstruction causes gastric distension and vomiting
  • later–anorexia, weight loss (UP)
88
Q

Say you have an acquired pyloric obstruction from ulceration, how should it be treated?

A
  • gastric drainage
  • PPI or H2 receptor agonist such as cimetidine
  • fluids
  • electrolytes
  • parental hyperalimentation if malnourished
89
Q

Say you have a pyloric obstruction from a carcinoma—what are your treatment options?

A

may require surgery or stent placement

90
Q

What are the clinical manifestations of intestinal obstruction?

A
  • diaphoresis
  • hypotension
  • nausea
  • vomiting
  • colicky pain
  • abdominal distension
91
Q

How do you evaluate intestinal obstruction?

A
  • clinical manifestations
  • ultrasound
  • radiography
92
Q

How do you treat intestinal obstruction?

A

Usually requires immediate surgical treatment

93
Q

What is gastritis?

A

A nonspecific inflammatory disorder of the gastric mucosa. (UP 7th)

94
Q

What causes acute gastritis?

A
  • medication (aspirin, ibuprofen, naproxen, indomethacin)
  • chemicals
  • Helicobacter pylori
95
Q

How does gastritis manifest clinically?

A
  • Vague abdominal discomfort
  • Epigastric tenderness
  • Bleeding (UP 7th)
96
Q

How do you treat acute gastritis?

A
  • NB: Tends to heal spontaneously within a few days–but healing can be facilitated
  • Discontinue injurious drugs
  • Use antacids
  • Decrease stomach acid secretion with H2-receptor antagonists (UP 7th)
97
Q

How is erosive gastritis treated?

A

pantaoprazole

98
Q

What is peptic ulcer disease?

A

A break or ulceration in the protective mucosal lining of the lower esophagus, stomach or duodenum. (UP)

99
Q

So what’s so bad about peptic ulcer?

A

Breaks in protective mucosal lining exposes submucosal areas to gastric secretions and autodigestion.

100
Q

What factors place someone at risk of developing peptic ulcer?

A

• Smoking tobacco
• Drinking alcohol
• Using NSAIDS habitually
• Getting older
• Carrying chronic disease (emphysema rheumatoid arthritis, cirrhosis, DM)
• Carrying infection of the gastric and duodenal mucosa with Helicobacter pylori (paraphrased from UP)

101
Q

What are the clinical manifestations of peptic ulcer?

A
  • Chronic intermittent pain in the epigastric area after eating
  • Vomiting
  • Anorexia
  • Weight loss
102
Q

What measures treat peptic ulcer?

A
  • Antacids
  • Suppression of acid secretion
  • Metronidazole or clarithromycin
  • Surgical intervention if necessary
103
Q

What is appendicitis?

A

Inflammation of the vermiform appendix, which projects from the apex of the cecum

104
Q

Who gets appendicitis?

A

People 20-30 years of age.

105
Q

How does appendicitis manifest clinically

A
  • Epigastric or periumbilical pain that may shift to the right lower abdominal quadrant
  • Nausea, vomiting
  • Fever
106
Q

How is appendicitis diagnosed?

A
  • Physical examination of location of pain
  • Elevated WBC count
  • May be confirmed by imaging (abdominal radiography, CT scan, ultrasound)
107
Q

How do you treat appendicitis?

A

Surgical intervention.

108
Q

How do alterations of platelets and coagulation affect hemostasis?

A
  • They prevent blood clotting (internal bleeding)
  • They cause clotting to occur when it is not needed (thromboembolic disease)
109
Q

Name the three broad categories of platelet disorders with a couple supporting numbers.

A
  • Too few platelets (thrombocytopenia, <100,000 platelets/mm3)
  • Too many platelets (thrombocythemia, >600,000/mm3)
  • Defective platelets (increased bleeding time with platelet count wnl)
110
Q

What may produce thrombocytopenia?

A
  1. Viral infections (EBV, rubella, CMV, HIV)
  2. Nutritional deficiencies (vitamin B12, folic acid, iron)
  3. Bone marrow replacement
  4. Medications (heparin, thiazides, estrogens, quinines)
  5. Chemotherapy
  6. Substance abuse (alcohol, cocaine)
111
Q

How does thrombocytopenia manifest?

A
  • Minor: petechiae and purpura on skin
  • Major hemorrhage from mucosal site (epistaxis, hematuria, menorrhagia, bleeding gums)
  • Rarely: intracranial bleeding or other sites of internal bleeding (UP 7th ed)
112
Q

What establishes diagnosis of immune thrombocytopenic purpura?

A
  1. History of bleeding
  2. Associated symptoms: weight loss, fever, headache
  3. Type, location, and severity of bleeding
  4. Evidence of infections (bacterial, HIV, and other viral)
  5. Medication history
  6. Family history
  7. Evidence of thrombosis
  8. Complete blood count and peripheral blood smear (UP 7th edition)
113
Q

How should thrombocytopenia be treated?

A
  1. Glucocorticoids (e.g., prednisone, which suppress immune response and prevent sequestering and further destruction of platelets)
  2. Intravenous immunoglobulins (IV Ig–to prevent major bleeding)
  3. Splenectomy should be considered if there is no response to therapy–to remove site of platelet destruction
  4. If nothing works and condition of patient is life-threatening–aggressive immunosuppressive medications (UP 7th edition)
114
Q

What causes thrombocythemia?

A
  • Exact cause unknown
  • May occur following
    –splenectomy
    –infection
    –inflammatory conditions
115
Q

How does thrombocythemia most commonly present?

A

As microvasculature thrombosis (erythromyalgia)–warm, congested red extremities with painful burning sensations, particularly in the fingers and toes

116
Q

How does one treat essential (primary) thrombocythemia?

A
  • Hydroxyurea (to suppress platelet production)
  • IFN (interferon–has side effects)
  • Anagrelide (interferes with platelet maturation)
  • Low-dose aspirin (alleviate erythromyalgia)
    (UP 7th ed)
117
Q

Name the alternations of platelet function.

A
  1. Disorders of platelet adhesion–deficiency of platelet membrane glycoprotein complex Ib/IX
  2. Disorders of platelet aggregation–failure to build fibrinogen bridges
  3. Disorders of platelet secretion–platelets aggregate, then disaggregate
  4. Disorders of procoagulant activity–lack of procoagulant factors
118
Q

What causes disorders of coagulation?

A

Defects or deficiencies in one or more of the clotting factors

119
Q

Why is vitamin K deficiency a problem?

A

Vitamin K is necessary for synthesis and regulation of prothrombin

120
Q

How does one treat vitamin K deficiency?

A

Parenteral administration of vitamin K.

121
Q

How does liver disease affect coagulation?

A
  • Decreases availability of clotting factors II, VII, and IX
  • May result in an increase in fibrinolytic activity
122
Q

How does DIC affect coagulation?

A
  • Results in unregulated release of thrombin and fibrin formation
123
Q

Where in the body is DIC located?

A

DIC may be localized to one specific organ or may be generalized to multiple organs.

124
Q

What conditions raise the risk of DIC?

A
  • Arterial hypotension, usually accompanying shock
  • Hypoxemia
  • Acidemia
  • Stasis of capillary blood flow
125
Q

What’s the most common cause of DIC?

A

Sepsis.

126
Q

What are petechiae?

A

Minute (1-2 mm) hemorrhages into skin and mucous membranes

127
Q

What conditions are associated with the appearance of petechiae?

A
  • Locally increased intravascular pressures
  • Low platelet counts
  • Defective platelet function
  • Deficiencies in clotting factors
128
Q

What are purpuras?

A

Small (3-5 mm) hemorrhages associated with many of the same disorders as petechiae

129
Q

What conditions are associated with the appearance of purpura?

A
  • Locally increased intravascular pressures
  • Low platelet counts
  • Defective platelet function
  • Deficiencies in clotting factors
  • Trauma
  • Vasculitis
  • Increased vascular fragility
130
Q

What are ecchymoses?

A

1-2 cm subcutaneous hematomas that begin as bruises that are red-blue, then blue-green, and later golden brown

131
Q

When should cervical spine injury be suspected with conscious patients?

A

When neck pain and weakness follow a trauma

132
Q

What signs in unconscious patients should raise suspicion of cervical spine injury?

A
  • Respiratory weakness
  • Extremity weakness without facial weakness
  • Hypotension with bradycardia
  • Difficulty maintaining normothermia
133
Q

Patients with injuries below C4 with breathe just fine, right?

A

Patients with injuries below C4 may initially breathe adequately but then progress to ventilatory failure.

134
Q

How should diagnosis of spinal cord injury be confirmed?

A

Plain radiographs or CT scan.

135
Q

How should suspected spinal cord injury be managed initially?

A
  • Immobilize spine with cervical collar, backboard
  • Administer oxygen as needed
  • Monitor patient carefully for signs of ventilatory failure–decreasing spontaneous Vt, VC, NIF
136
Q

Describe rhabdomyolysis.

A
  • A condition in which damaged skeletal muscle tissue breaks down rapidly.
  • Breakdown products of damaged muscle cells are released into the bloodstream.
  • Some of these, such as the protein myoglobin, are harmful to the kidneys and may lead to renal failure.
137
Q

Clinical presentation of rhabdo may include what symptoms.

A

• Muscle pains
• Vomiting
• Confusion
(Kettering)
• Malaise
• Fever
• Tachycardia
• Abdominal pain
• Altered mental status (from underlying etiology)
(UTD)

138
Q

What situations should raise suspicion for crush injury?

A
  • When patients have been trapped immobilized.
  • When large muscles have been injured.
  • When prolonged compression has occurred.
  • When vascular compromise is present.
139
Q

How is rhabdomyolysis treated?

A
  • Intravenous fluids
  • Dialysis or hemofiltration in severe cases
    (Kettering)
    • Recognition and management of fluid and electrolyte abnormalities
    • Identification of the specific causes and the use of appropriate countermeasures directed at the triggering events, including discontinuation of drugs or other toxins that may be etiologic factors
    • Prompt recognition, evaluation, and treatment of compartment syndrome in patient in whom it is present
    (UTD)
140
Q

Complications of rhabdomyolysis

A

• Fluid and electrolyte abnormalities
• Acute kidney injury
• Compartment syndrome (may develop after fluid resuscitation, with worsening edema of the limb and muscle)
• Disseminated intravascular coagulation (DIC) (infrequent—from release of tromboplastin and other prothrombotic substances from the damaged muscle)
• (Potential cardiac abnormalities from hyperkalemia)
(Kettering and UTD combined)

141
Q

Describe compartment syndrome

A

Swelling of damaged muscle leading to compression of such surrounding tissues as nerves and blood vessels that share the fascial compartment.

142
Q

How can compartment pressures be monitored?

A

Using a needle with a manometer.

143
Q

When is fasciotomy indicated?

A

When compartment pressure exceeds 30 mmHg.

144
Q

What does CIP stand for?

A

Critical Illness Polyneuropathy

145
Q

What are CIP and CIM?

A

Overlapping syndromes of of widespread muscle weakness and neurological dysfunction that can develop in critically ill patients receiving intensive care.

146
Q

So how are CIP and CIM distinguished from one another?

A

They have similar symptoms and presentations; they are distinguished largely on the basis of specialized electrophysiologic testing and muscle and nerve biopsy.

147
Q

What causes CIP/CIM?

A

Unknown–though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome.

148
Q

What factors contribute to the development of CIP/CIM?

A

Corticosteroids and neuromuscular blocking agents may contribute to the development of CIP/CIM.

149
Q

What does CIM stand for?

A

Critical Illness Myopathy

150
Q

Can anything be done about CIP/CIM?

A

Early physical therapy may enhance recovery of muscle strength.

151
Q

2018 Surviving Sepsis 1-hr bundle

A
  • Measure lactate level. Remeasure if lactate is >2 mmol/L
  • Obtain blood cultures prior to administration of antibiotics.
  • Administer broad-spectrum antibiotics.
  • Begin rapid administration of 30mL/kg crystalloid for hypotension or lactate >=4 mmol/L.
  • Apply vasopressors if patient is hypotensive during or after fluid resuscitation to maintain MAP >=65mmHg.
152
Q

2012 Surviving Sepsis goals of initial resuscitation

A
  • CVP 8-12 mmHg
  • MAP >= 65 mmHg
  • Urine output >= 0.5 mL/kg/hr
  • SvO2 >= 70%
153
Q

2017 Surviving Sepsis definition of sepsis

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection.

154
Q

2017 Surviving Sepsis definition of septic shock

A

A subset of sepsis with circulatory and cellular/metabolic dysfunction associated with a higher risk of mortality

155
Q

How prevalent is appendicitis?

A
  • Most common surgical emergency of the abdomen
  • Affects 7-12% of the population
156
Q

What is a thrombus?

A

• A clot attached to the vessel wall.
• Arterial clots form under conditions of high flow and composed mainly of platelet aggregates held together by fibrin strands.
• Venous clots form in conditions of low flow and are composed mostly of red cells with larger amounts of fibrin and few platelets.

157
Q

What is the Virchow Triad?

A

1) Injury to the blood vessel endothelium
2) Abnormalities of blood flow
3) Hypercoagulability of the blood

158
Q

UTD general principles for the acute management of STEMI.

A

●Relief of ischemic pain
●Assessment of the hemodynamic state and correction of abnormalities that are present
●Initiation of reperfusion therapy with primary percutaneous coronary intervention (PCI) or fibrinolysis
●Antithrombotic therapy to prevent rethrombosis or acute stent thrombosis
●Beta blocker therapy to prevent recurrent ischemia and life-threatening ventricular arrhythmias

159
Q

What laboratory findings accompany rhabdomyolysis?

A

• Most notably—CK levels at lead 5x upper limits of normal, ranging from approx 1500->100,000 IU/L
• Myoglobinuria, which may or may not be visible to naked eye
• Hyperkalemia (release of potassium from damaged muscle cells)
• Hyperphosphatemia (release of phosphate from damaged muscle cells)
• Hypocalcemia (occurs in first few days
• Hyperuricemia
(UTD)

160
Q

What are schistocytes?

A

Fragmented parts of red blood cells ; they are typically irregularly shaped, jagged, and pointed on two ends. (W)

161
Q

Name several causes of schistocytes.

A
  • Disseminated intravascular coagulation generates fibrin strands that sever red blood cells as they move past a thrombus
  • Hemolytic anemia, formed through artificial heart valves
    (W)
  • Damaged blood vessels form schistocytes as blood cells flow through small vessels (FMD)
162
Q

What conditions provoke osmotic diarrhea?

A
  • Deficiency of lactase or pancreatic enzymes
  • Excessive ingestion of synthetic, non-absorbable sugars
  • Ingestion of full-strength tube-feeding formulae
  • Dumping syndrome associated with gastric resection (UP 7th)
163
Q

What conditions cause secretory diarrhea?

A
  • Viral infections such as rotavirus
  • Bacterial enterotoxins such as Escherichia coli and Vibrio cholerae
  • Exotoxins from from overgrowth of Clostridium difficile after antibiotic therapy
  • Small bowel bacterial overgrowth (UP 7th)
164
Q

What conditions provoke motility diarrhea?

A
  • Resection of small intestine (short bowel syndrome)
  • Surgical bypass of an area of the intestine
  • Fistula formation between loops of intestine
  • Irritable bowel syndrome–diarrhea predominate
  • Diabetic neuropathy
  • Hyperthyroidism
  • Laxative abuse (UP 7th)
165
Q

What is immune thrombocytopenic purpura?

A

An acquired thrombocytopenia caused by autoantibodies against platelet antigens (UTD accessed 20200619)

166
Q

What is SEPS?

A

Minimally invasive Subdural Evacuation Port System (Medtronic website accessed 20200821)

167
Q

SEPS details.

A
  • Offers minimally invasive subdural evacuation to relieve brain compression
  • Uses 5mm burr hole smaller than invasive systems
  • Evacuating port does not enter subdural space
  • Can be done at bedside
    (Medtronic website accessed 20200821)

accs (13 decks)

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