Critically Ill patient Flashcards

1
Q

Stress ulcer prophylaxis

A

oral PPI, or IV H2 blockers or oral antacids. Depends on if pt can eat.

Stop prophylaxis after extubated and doing well.

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2
Q

Risk factors for stress ulcer

A

Hx of GI bleeding in past year, evidence of coagulopathy, mechanical ventilation >48 hrs, severe CNS injury (TBI or spinal cord injury) , severe burns, combination of sepsis, prolonged ICU stay and high dose steroid use for greater than one week.

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3
Q

When to order ancillary tests to confirm brain dead

A

unable to examin cranial nerves
pts with neuromuscular paralysis or heavy sedation, unable to complete apnea test or inconclusive results, numerous confounding variables (multiorgan failure)

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4
Q

Neuro examination of a brain dead patient

A

comatose pt
absent cranial nerve reflexes and motor responses (including flexor or extensor posturing)
absent oculovestibular reflex (caloric response)
absent cough with tracheal suctioning
absent sucking or rooting reflexes
apnea by apnea test

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5
Q

clinical criteria for someone who is brain dead

A

lack of spontaneous respirations
CT MRI with devastating CNS event or known cause
absent of confounding factors (sedative medications or metabolic or HDS derangements)
no confirmed confounding drug intoxication or poisoning
core temperature >36 and systolic BP >100

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6
Q

what is the apnea test?

A

confirms brainstem failure if the patient cannot generate spontaneous breaths or triggers ventilators in response to elevated PaCO1 levels >10 minutes after disabling control mode

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7
Q

what to do based on bedside apnea test?

A

negative - pt is not brain dead
inconclusive or pts is unable to tolerate - needs ancillary testing
positive - repeat clinical exam and if suggestive of brain dead then patient is clinically brain dead. If repeat exam is non conclusive needs ancillary testing.

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8
Q

positive apnea test is defined as

A

no spontaneous respirations for approximately 10 minutes and ABG must confirm PaCO2>60 mmHg or have increased >20 mmHg from baseline ABG.

if spontaneous respirations are observed and the patient is not brain dead

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9
Q

gold standard for brain dead confirmation

A

cerebral blood flow testing - cerebral angiogram but this is highly invasive and not routinely done and never as a first step in diagnosing. Can be used if having difficulty distinguishing if braindead

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10
Q

DO we use EEG or ECI for brain death confirmation?

A

no because it’s is suspecepitble to excessive artifact from other electronic defices in ICU and so less reliable. Also very sensitive to effects of sedative medications and metabolic derangements and so can be confounded.

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11
Q

do we use the atropine response test

A

no. IT’s not been validated in confirming brain dead

it’s supposed to see increase in heart rate by 3% via the vagus nerve which is the last brain functions lost

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12
Q

nutritional support in critically ill pts

A

enteral nutrition is preferred
start enteral nutrition in 24-48 hrs and advance to goal over 48-72 hrs
Gastric feeding preferred
Jejunal feeding if intolerance to gastric feeding or high risk for aspiration prokinetic agents if feeding intolerance

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13
Q

when to hold enteral nutriition?

A

if hypotensive and escalating doses of vasopressors

or decreased intravascular volume due to risk for bowel ischemia

Absence of bowel sounds or flatus is not a contraindication to early enteral feeding even in pts who have undergone surgery for bowel perforation

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14
Q

When do we use post pyloric feeding tubes?

A

in patients who are at high risk for aspiration.

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15
Q

when do we start parenteral nutrition?

A

can be started after 7 days if EN is not feasible.

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16
Q

what is parenteral nutrition associated with?

A

hyperglycemia, hypertriglyeridemia and intestinal mucosal atrophy and increased risk for infections.

17
Q

when and how much to give patients IV corticosteroids?

A

hydrocortisone 200-300 mg/day if there’s adrenal insufficnecy

18
Q

Surviving Sepsis and early goal directed therapy include:

A

CVP pressure of 8-12 mmg, MAP>65 mmg, central venous oxygen sat>70% and urine output 0.5 ml/kg/hr

19
Q

what causes pneumothoraces?

A

can be spontaneous or iatrogenic. Nonspontaneous include trauma and from positive pressure ventilation, CVC, thoracentesis.

20
Q

Treatment of large pneumothorax

A

Chest tube.

If shows signs of hypotension, tachycardia and hypoxemia need urgent decompression of pleural space with needle. Place at 2nd intercostal space.

21
Q

what helps to reduce incidence of stress ulcers?

A

early enteral feeding alone

22
Q

Who gets stress ulcer prophylaxis?

A

1 or more of the RF mentioned gets prophylaxis.

23
Q

When to start enteral nutrition in a critically ill but hemodynamically stable pt is:

A

start within 48 hrs has been shown to improve outcomes.

DON’T start in hemodynamically unstable pts due to risk for bowel ischemia.

24
Q

complication of pneumothorax

A

can see obstructive shock happen with decreased cardiac output from poor venous return in setting of high intrathoracic pressures and impaired cardiac pumping from compressed ventricles.

25
Q

presentation of pneumothorax:

A

dyspnea, pleuritic chest pain, tachypnea, hypoxia, and decreased breath sounds affected side

see hyperresonance to percussion

26
Q

If pt who has pneumothorax that involves <20% of chest then pt can be

A

observed for 24 hrs with oxygen as needed

repeat imaging in 24 hrs.

if Pnuemothorax is gone then can be discharged with 48 hr follow up

if persistence of pneumothorax is still there without progression pt can be discharged with follow up in 48 hrs

27
Q

chest tube for pnuemothorax is:

A

progression from initial CXR

initial pneumothorax >20% or if pt develops severe sympotms

28
Q

how to know when to remove a chest tube?

A

need to look for airleak

if none ok to take out chest tube.

if present then need to repeat checking in one day (24 hrs later) after getting CXR

if this persists consider getting a CT surgery consult.

29
Q

what is a side effect or complication on being on prolonged PPI for stress ulcer prophylaxis

A

increased risk for nosocomial pneumonia

PPI can reduce gastric acid and promote bacterial growth and with GERD can lead to colonization of endotracheal tube and increase risk of pneumonia.

30
Q

who gets spontaneous pneumothorax

A
tobacco use
Marfan syndrome
homocystinuria
thoracic endometriosis 
family history
31
Q

mild cases of pneumothorax definition and management

A

2-3 cm of trapped areas
managed conservatively with observation for 6 hrs

give supplementary oxygen until symptoms resolve and repeat CXR shows stability and resolution of the pneumothorax

32
Q

what is hypoxic ischemic encephalopathy (HIE) is a syndrome

A

acute global brain injury resulting from critical reduction or loss of blood flow.

most common clinical presentations include disorders of consciousness, seizures, and myoclonus.

33
Q

when does spontaneous pneumothorax happen?

A

in young and otherwise healthy patients can be tolerated