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NICU > Repetera-utvalda > Flashcards

Repetera-utvalda Flashcards

1
Q

ASA I (all surgery)

A

*Normal, healthy patient.
*0.08 % mortality within 48h
*0.06% mortality within 7 days

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2
Q

ASA II (all surgery)

A

II - mild systemic disease, no functional limitation
*0.27% mortality within 48h
*0.4% mortality within 7d

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3
Q

ASA III (all surgery)

A

III - severe systemic disease, definitive functional limitation
*1.8% mortality within 48h
*4.3% mortality within 7d

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4
Q

ASA IV (all surgery)

A

IV - severe systemic disease that is a constant threat to life
*7.8% mortality within 48h
*23.4% mortality within 7d

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5
Q

ASA V (all surgery)

A

V - moribund, expected to die within 24h with or without surgery.
*9.4% mortality within 48h
*50.7% mortality within 7d

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6
Q

ASA VI (all surgery)

A

VI- organ donor

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7
Q

WHat does the appendix “e” stand for in the ASA classification?

A

It means that emergency surgery is associated with 3x the risk compared to the given ASA % that are stated for elective surgey.

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8
Q

what factors determines CPP?

A

Cerebral perfusion pressure
- intact ?
- Blood pressure.
- ICP

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9
Q

Where should the srterial IV line be calibrated?

A

By meatus to etter reflect the intracranial BP.

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10
Q

What is the most potent cerebral vasodilator?

A

CO2.

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11
Q

What does hyperventilation create?

A

*Decreased CBV
*Decreased CBF

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12
Q

What is ETCO2?

A

End tidal Co2

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13
Q

How does ETCO2 correlate to arterial CO2?

A

Usually ETCO2 is approximately 5mmHg lower than in arterial blood.
The goal is PaCO2 30-35.

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14
Q

What has to be thought of in prone position?

A

Excessive fluids can contribute to facial edema and PION in the worst case.

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15
Q

Why should inhalation anesthesia be avoided?

A

They REDUCE central metabolism by suppressing neuronal activity.
That might sound good BUT
They DISTURB CEREBRAL AUTOREGULATION and cause cerebral vasodilation.

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16
Q

What drug is generally used for induction?

A

Propofol.
*unknown action. - but works as a sedative hypnotic.
*Short 1/2 life.
*no active metabolites.

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17
Q

When Propofol is used as TIVA- total intravenous anethesia- What does it do to MAP and ICP?

A

It causes dose-dependent decrease in mean arterial blood pressure MAP and ICP.
* reduces CMRO2
* Reduces CBF and ICP
* Short 1/2 life.

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18
Q

What barbiturate is usually used in induction?

A

Sodium thiopenthal.
* Rapid onset
* Short acting
* minimal effect on ICP, CBF and CMRO2

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19
Q

What is the mechanism of Ketamine?

A
  • Its an NMDA receptor antagonist
  • It produces dissociative anesthesia.
  • Maintains cardiac output.
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20
Q

Positives and NEGATIVES with nonsynthetic narcotics - morphine

A

+ : Increase CSF absorption and minimally reduce cerebral metabolism.
- :
* Cause dose-dependent respiratory depression —hypercarbia in the non-ventilated patient.
*N/V postop.
* Cause histamine release
* Can accumulate in renal or hepatic insufficient patient and cause confusion

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21
Q

What is good with synthetic narcotics?

A

They do not cause histamine release.

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22
Q

Name two synthetic narcotics prominently used in neurosetting

A
  • Fentanyl
  • Remifentanil (ultiva)
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23
Q

Name two commonly used paralytics

A
  • Succinylcholine
  • Rocuronium
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24
Q

What side-effects make succinylcholin non-preferable in injuries or children/adolecsens?

A

Extra risk of Malignant hyperthermia.

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25
Q

What are anesthetic requirements for intraoperative evoked potential monitoring?

A

INDUCTION:
* Minimize pentothal or use etomidate
*! Use TIVA NOT inhalation.
+ Obs nondepolarizing muscle relaxants have little effect on evoked potentials!
+ Propofol has mild effect on evoked potentials,
*continous infusion should be used, not boluses.
* Obs! SSEPs can be affected by hyper or hypothermia and by changes in BP.
+ Hypocapnia, down to end tidal CO2 21 has no effect on peak latencies
+ Antiepileptic drugs have NO effect on SSEPs.

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26
Q

What is the incidence of Malignant hyperthermia?

A

Peds: 1:15000
Adults: 1:40000

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27
Q

Treatment of Malignant hyperthermia?

A
  • Eliminate offending agent
  • DANTROLENE SODIUM - 2.5mg/kg iv up to 10mg/kg until symtoms subside.
  • Hyperventialtion w 100% oxygen.
  • Cooling
  • Bicarbonate for acidosis
    Procainamide for arrythmias
  • Diuresis - volume loadinga nd osmotic diuresis.
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28
Q

Why is hyperglycemia a bad thing?

A

It exacerbates ischemic deficits

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29
Q

What can be done to protect against ischemic injuries?

A
  • Lower CMRO2
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30
Q

What is the putative mechanism of Neurogenic stress cardiomyopathy?

A

Cathecholamine surge. Possibly in myocardial sympathethic nerves. As a result from hypothalamic stimulation or injury from SAH.

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31
Q

When is the peak incidence of neurogenic stress cardiomyopathy after aSAH?

A

2 days-2weeks after SAH.

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32
Q

What treatment does greenberg suggest for neurogenic stress cardiomyopathy?

A

Dobutamine
Milrinone.

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33
Q

What is the normally used name for Neurogenic stress cardiomyopathy and what nickname is it often given?

A

Takotsubo cardiomyopathy.
The nickname is “broken heart syndrome”.

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34
Q

When can neurogenic pulmonary edema occur?

A
  • SAH
  • generalized seizures
  • head injury.
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35
Q

What are the two possibly synergisic explanations to neurogenic pulmonary edema?

A
  1. sudden ICP raise or hypothalamic injury with sympathetic discharge cause redistribution of blood to the pulmonary circulation. An eleveation of pulmonary capillary wedge pressure occur and increased permeability of the capillaries too.
  2. Cathecholamines disrupt the capillary enothelium which increases alveolar permeability.
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36
Q

What is the treatment of pulmonary edema?

A
  • Low levels of PEEP
  • NOrmalization of ICP
    A PA catheter is useful
    *SOmetimes Dobutamine and Furosemide might help.
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37
Q

What is the advantage of dobutamine to previously attempted alpha and beta blockers?

A

Dobutamine does not reduce cerebral perfusion.

38
Q

what is critical illness polyneuropathy?

A
  • Affects primarily distal muscles
  • precense of sepsis, multiorgan failure, respiratory failure or septic inflammatory response syndrome - SIRS.
  • Difficulty weaning from ventilator or extremity weakness.
  • EMG show low amplitudes of compound muscle action potentials and SNAP.
  • widespread muscle denervation potentials
  • normal or only mild increase in serum CPK levels.

—–Recovery occurs in weeks to months—-faster than Guillian Barre, –treatment is supportive. Complete recovery 50%

39
Q

What is SIADH?

A

Euvolem or Hypervolem Hypothonic Hyponatremia

40
Q

Define hypotone

A

serum osmolality under 275mOsm/kg

41
Q

What is a high urinary osmolality?

A

Over 100 mOSm/kg

42
Q

What is Cerebral Salt Wasting?

A

SIADH but with ExtraCellular Fluid Depletion due to renal sodium loss.

43
Q

What is abnormally high koncentrations of Na in urine?

A

More than 20 mEq/l

44
Q

What disease is important to rule out when accessing suspected SIADH and/or cerebral salt wasting?

A

Hypotyreoidism. - Take an TSH.

45
Q

Other than TSH, what is the minimum work up for suspected SIADH or cerebral salt wasting?

A
  • Serum Na, Urine Na, Serum osmolality, and clinical assessment of volume status.
46
Q

What is the risk of overly rapid correction of low serum sodium?

A

Osmotic demyelination; Pontine myelinolysis

47
Q

Normal range of serum osmolality

A

282-295.

48
Q

Panic values of serum osmolality

A

under 240 and over 321.

49
Q

Fatal range of serumosmolality

A

over 420.

50
Q

What is the risk of treating SIADH patients with fluid restriction in a neurosurgical setting?

A

If the diagnosis is wrong and the real etiology is CSW, the patient is actually volume depleted and need volume replacement with Na.

51
Q

What is the most common type of hyponatremia after neurosurgery?

A

SIADH - syndrome of inappropriate Antidiuretic hormone secretion.

52
Q

SIADH is associated to different types of tumors and also to a specific type of surgery. Which?

A

Transsphenoidal

53
Q

CSW is common after aneurysmal SAH. How common is it compared to SIADH?

A

CSW: 6-23%
SIADH: 35%

54
Q

What endocrine disturbances might induce SIAD?

A
  • Hypothyreoidism
  • Adrenal insufficiency
55
Q

What “miscellaneous” reasons might induce SIAD?

A
  1. Anemia
  2. Stimulation of ADH release:
    * Stress
    * Severe pain
    * Nausea
    * Hypotension
    * (postoperative state)
  3. Acute intermittent porphyria
56
Q

Name a common “neurosurgery-hormonal” drug that is an ADH analogue

A

Oxytocin - ADH cross activity.

57
Q

When can hypERtonic hyponatremia occur in a neurosurgical setting? 2 common scenarios

A
  1. Hyperglycemia - for every 100mg/dl increase of glucose, Na decrease by 1.6-2.4 mEq/dl.
  2. Mannitol
58
Q

What is the result of inappropriate ADH stimuli?

A
  • Urine koncentration and elevated urine osmolality
  • Expansion of extracellular fluid volume (as the Na konc is so low in the blood)
    For unclear reasons edema does not occur.
59
Q

How do we check for normal adrenal function?

A
  • No hypotension
  • No hyperkalemia
60
Q

What do we do in case of suspected dehydration in patients where a SIADH was expected?

A

We then belive in CSW instead and treat with rehydration and Na.

61
Q

What is done if a patient with suspected SIADH has a serum Na of under 124 and/or clinical signs of hyponatremia

A

We give Na (konc dependent on how fast the hyponatremia occured) and measure arterial levels q2-4 hours.
If the patient is obvious hypervolemic and does not have hypotension or hyperkalemia, furosemide might also be given.

62
Q

What are signs of fast developing hyponatremia?

A
  • neuromuscular excitability
  • cerebral edema
  • muscle twitching and cramps
  • N/V
  • Confusion
  • Seizures
  • Resp arrest
  • Permanent neurologic injury/coma/death
63
Q

What causes Diabetes insipidus

A
  • Low levels of ADH.
  • Rarely - renal insensitivity to ADH.
64
Q

Signs of Diabetes insipidus and risks with diabetes insipidus?

A

Sign= watercraving and polyuria w low urine osmolality.
Risk= Severe dehydration

65
Q

What are the two etiologies of Diabetes insipidus?

A
  • Central or Neurogenic.
  • Nephrogenic
66
Q

Where in the brain is a damage situated that causes diabetes insipidus?

A

In the hypothalamic-pituitary axis

67
Q

What neurosurgical situations may involve diabetes insipidus?

A
  • Posttraumatic - incl surgery
  • Tumor ….craniopharyngeoma, lymphoma, mets
  • Granuloma; neurosarcoidosis, histiocytosis
    *Aneurysms
    (and non-neurosurgical like infection, autoimmune, familial, idiopathic)
68
Q

When is transient diabetes insipidus seen?

A

After transsphenoidal surgery/removal of craniopharyngeoma

69
Q

What is the treatment of DI?

A

Desmopressin (Vasopressin analogue).

70
Q

How do I know its DI in the clinical setting?

A
  1. Typical clinical signs
  2. urine output more than 250cc/hour.
  3. Normal or above normal Na.
  4. Normal adrenal function
  5. Urine osmolality usually between 50-150mOsm/kg. Defined as below 200.
71
Q

What is normal urine osmolality?

A

between 500-800mOsm/kg

72
Q

WHY cannot DI occur in primary adrenal insufficiency?

A

Due to the need of the kidneys for at least minimum mineralcorticoid secretion to make free water.

73
Q
A
74
Q

What is the procedure for performing RASS?

A
  1. on observation, pt is alert, restless or agitated - score 0-+4
  2. If not alert; test verbal attention and ability to look at, shortly focus on or move/briefly open but no contact eyes. Score -3 to -1.
  3. If no response to verbal stimuli, shake shoulder or sternal rub. - -5 to -4.
75
Q

GCS

A

EYE
1-Does not open
2-Open to pressure
3-Open to sound
4-Spontaneously
VERBAL
1-
2-growns
3-Utter words but do not form sentenses
4-confused (not oriented but communicates coherently)
5-Spontaneously
MOTOR
1-None.
2-Extension
3-Abnormal flexion
4-Normal flexion
5-Localizes.
6-Obey command

76
Q

What is the CPP range for autoregulation of cerebral blood flow?

A

Its belived to be between 50 and 150 mmHg.

77
Q

What is the normal cerebral blood flow during autoregulation?

A

50ml/100g/min.

78
Q

What happens to the CBF when CPP go under 50mmHg?

A

It goes down.

79
Q

What happens to CBF when CPP goes over 150mmHg?

A

It goes up.

80
Q

What is CMRO2?

A

cerebral metabolic rate of oxygen consumption

81
Q

What is the CBF:CMRO2 ratio in quiescent brain?

A

14:18.

82
Q

How is the CBF calculated?

A

Its CPP/CVR or (MAP-ICP)/CVR

83
Q

How is CPP calculated?

A

Its MAP-ICP

84
Q

How is MAP calculated?

A

It is ((DBPx2)+SBP)/3

85
Q

In reality, what is CVR representing?

A

It the resistance of the cerebral vascular bed.

86
Q

When CPP is between 50-150mmHg, the CBF is kept constant. How?

A

The CVR is raised linear with the raised CPP of 50-150mmHg and in this way CBF is kept constant.
CBF= CPP/CVR as long as CPP is between 50-150mmHg.

87
Q

What two factors affect CVR and change it?

A
  1. PaCO2 - there is a linear raise of CBF with increase of PaCO2 between 20-80mmHg.
  2. CVR is affected by changes in CPP -changes in vessel tone is produced via a myogenic mechanism.
88
Q

WHat does a CBF of over 60 ml/100g tissue mean?

A

Hyperemia

89
Q

What does CBF of 16-18ml/100mg tissue mean?

A

EEG become flatline.

90
Q

What cerebral bloodflow causes alteration in cell membrane transport, cell death and stroke?

A

10ml/100g tissue

NICU (7 decks)

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