Critical care exam II notes
Female: 0.5-1.1 mg/dL or 44-97umol/L
Male: 0.6-1.2 mg/dL or 53-106 umol/L
*umol/L = SI units
Glasgow coma scale: (p. 356)
Total can be 3-15
Positive score (good):
13-15 is a good score to have.
<8 coma!!! ;(
Calculation of Cerebral perfusion pressure (CPP)
Optimal cerebral perfusion:
>13 on Glasgow coma scale
CPP maintained @ 70mm/Hg
- Absence of new neuro deficits
- Vital signs w/in normal limits
ICP should be maintained at
< 20 mmg/Hg
Cerebral pressure perfusion should be maintained at
ICP diagnosis concernes
* Still worry about the airway & breathing
Skull fracture: Linear
Most common type of fracture. Not serious unless extended to orbit, sinus or across a vessel.
* When there is an extension of fracture, the pt. is admitted for observation for signs of: intracranial bleeding & epidural hematoma.
Skull fracture: Basilar fractures
A linear fracture @ the base of the skull. This type of fracture is difficult to determine on x-ray & is diagnosed by clinical presentation to the pt. (raccoon eyes, Battles sign)
* Dural tears are very common w/basilar skull fractures & may lead to meningitis.
* Linear- looks like a line (on the skull)
Bruising behind the ear, rhinorrhea
Bilateral periorbital edema & bruising, and otorrhea.
Skull fracture: Depressed
Outer table of the skull is depressed inward below the inner table of surrounding intact skull.
* The dura may be intact, bruised or torn
* If dura is torn the brain is open to environment & meningitis can occur
* The compressed & bruised brain beneath the depressed bone or bone lodged in brain parenchyma is the source of focal neuro deficit & may cause seizure
Comminuted skill fracture
Occurs from many or multiple linear fractures w/a depressed area at the site of impact @ site of impact.
- Fracture radiates away from the impact site
- Referred to as "eggshell fracture"
- Risks are similar to those occurring w/depressed fracture (torn dura exposing brain to infection like meningitis, or bone lodged in brain, bruised brain).
All the above can lead to seizure or neuro deficit
Late= Cushing's triad- irreversible
Cushing's triad consists of HTN, w/widening pulse pressure, bradycardia & irregular respirations--> Irreversible
A. Monitor pt. w/GCS of 3-8 (coma)- used to monitor response to therapy such as after giving mannitol or to augment neuro assessment.
B. Devices placed in ventricles, parenchyma, or in subarachnoid, epidural & subdural spaces.
C. Ventriculostomy- Most common because it allows for interventions-> drains CSF, remove blood from subarachnoid hemorrhage.
Normal 60% to 70% Value <50% suggest cerebral ischemia.
Partial pressure of oxygen w/in brain tissue (PbtO2). Measured by placing monitor probe directly into the brain (damaged or damaged) white matter & attaching to stand alone monitor.
20mm/Hg or device specific
- CBC (emphasis on HCT, Hgb & platelets)
- Coag profile PT/INR, aPTT- because BI may induce coagulopathy.
- Electrolytes, BUN, Cr, Liver function, Serum osmolality.
Diagnostic testing for ICP & TBI
- CT scan (non contrast) to assess for worsening intracranial mass effect
- MRI anatomical detail to pathology contributing to increased ICP
- Cerebral blood flow monitoring- transcutaneous Doppler device measures velocity of arterial flow & allows for the indirect monitoring of CBF @ bedside
- Evoked potential monitoring- noninvasive, applying sensory stimuli & recording the electrical potentials created.
- EEG - to identify seizure activity or lack of electrical activity which may be consistent w/brain death.
Radiological studies/diagnostic test ICP
- Brainstem auditory evoked potentials= evaluation brainstem function, conducted on conscious/unconscious
- Somato sensory evoked potentials- measure peripheral nerve response- helpful in evaluation spinal cord function.
Evoked potential monitoring
Stroke assessment: in ED
Witness description of symptoms, ID of exact time symptoms started & a neuro assessment.
- Eval mental status (LOC arousal, oritentation)
- Cranial nerve function motor strength, sensory function, nerve function
- Motor strength
- Sensory function
- Deep tendon reflexes
NIHSS is use:
To assess severity of presenting signs/symptoms, especially if pt.'s is a candidate for a thrombolytic therapy.
* One side of face or body is weak, limp or numb (or all)
* Slurred speech & Inability to comprehend what's said
* Visual disturbance, transient loss of vision 1 or both eyes
* Double vision or visual field deficit
* Sudden onset of severe HA "worst HA of my life"
- VS q 15min for first 6 hrs
- BP elevations is common in stroke pt.
Reducing BP can lower blood flow & O2 to the ischemic brain tissue. A gradual 20% lowering of the BP is recommended to prevent enlargement of infarcted area & worsening the neurological deficit.
Spinal cord injury (SCI): Priority intervention
Head in proper alignment, collar placed.
Cervical injury affects _____.
Phrenic nerve impairment, tx w/phrenic nerve pacemaker.
* VERY IMPORTANT FOR BREATHING!
Intact diaphragmatic breathing, w/varying impairment of intercostal and abdominal muscle function.
Spinal cord Injury assessment:
* Respiratory and Neurological are the 1st assessment priority!
- Neuro assessment includes: motor, reflex, sensory responses.
- Assessment of major muscle groups & sensory level is completed to determine level of injury.
- Neuro assessments are done q 15mins & report any change to the doctor
To prevent further trauma use 3 people to turn and stabilize head and neck when moving them.
Can develop fecal impaction, monitor for BM and supply daily stool softener.
Electrical silence of the cord below the level of injury that causes complete loss of motor, sensory & reflex activity.
- Begins minutes after an injury and lasts 4-6wks. Permanence of injury is unknown until spinal shock is resolved.
- Resolution is signaled by return of the deep tendon reflexes
Disruption of the autonomic pathways, resulting in temporary loss of autonomic function below the level of injury.
Sympathetic input is lost, causing vaso dilation & distributed shock, which manifests as:
- Bradycardia- may be sever enough for a temp pacemaker
Duration varies & resolution is signaled by return of sympathetic tone
What type of diuretic is used for head injury?
Mannitol- It is osmotic, pulls water from brain interstitium into plasma.
* Used to treat ICP
* Use inline filter to administer & check for crystals.
________ is a priority when looking at vital signs, DO NOT GLOSS OVER!
Neuro type pt.'s get ____ instead of saline bolus.
Why? Albumin is a volume extender.
Head injury- which vital sign is more important?
BP is more important than temperature- only if abnormal
Dilantin (Phenytoin): Action
- Use separate line
- Mixed w/NS only
Dilantin Dosages for Status epilepticus:
10-20mg/kg, IV in 0.9% NS only!
* Give over 20-30mins
* Do not exceed a total dose of 1.5g or 50mg/min
If doesn't work try another antiepileptic, barbiturate, or anesthesia.
* Don't give w/dextrose- give somewhere else!!
Dilantin maintenance dose:
100mg IV over 2mins q 6-8°
- ENSURE PATENT AIRWAY, MAINTAINS BREATHING & CIRCULATION
- Padding side rails
- Bed in low position
- If pt. in chair- safely lower them onto floor w/pillow under head
- Remove restrictive clothing & jewelry
Therapeutic Range:: Total: 10 to 20 mcg/ml.
Toxic level: >20-30 mcg/ml
1st choice medication for seizures:
*If it fails to stop seizure in 10mins or if intermittent seizure persists longer than 20mins try-> Phenytoin (Dilantin) or fosphenytoin (Cerebyx)
Autonomic dysreflexia (AD)
Medical emergency- can result in stroke, seizure or other complications.
* Occurs w/T6 or above after spinal shock resolved.
* Characterized by- exaggerated response of the sympathetic nervous system.
A. Severe HTN, HA and bradycardia
Assess & remove the cause
- Kinked urinary catheter
- Fecal impaction
- Tight clothing
- Extreme temps
- Elevate HOB
- Remain calm & supportive
For HTN give: Hydralazine, Clonidine or doxazosin, prazosin
What to do for admitting diagnosis for meningitis:
Assess for fever, cough
Have visitors put on PPE
Mannitol or hypertonic saline given
Ventriculostomy catheter to drain CSF
↑ HOB 30-40°
Clinical manifestations of Bacterial meningitis:
- Nuchal rigidity
* Kernig's sign: severe stiffness of the
hamstrings, inability to straighten leg.
* Brudzinski's sign: Sever neck stiffness,
causes him & knees to flex when neck is
- infection of the pia & arachnoid layers
Glucose <70 mg/dL
AKA insulin shock or Insulin reaction
1st clinical sign- ↓mental status change
ANS stimulations: Activates SNS-> release of epinephrine
- Nervousness, apprehension, tremors
- Tachycardia, palpitations, tremors
- Dilated pupils
- Fatigue & weakness
- Difficulty speaking/thinking
- Difficulty walking
- Visual disturbances (double vision, field deficit
- Altered consciousness (coma, convulsions, seizure
- Maniacal behavior (acute paranoia or catatonia)
DKA- diagnostic labs
- Blood glucose average 675 & more
- UA- Ketones, ↑BUN
- ABG's ↓pH <7.30, ↓bicarb
- CMP electrolytes: k+, mg & phosphorous
- CBC: for plasma
Type 1 DM mostly (can see with DM II)
* Hyperglycemia due to increased glucose production & decreased utilization
* Altered k+ balance (must watch)
* Excess acids result in ↑ anion gap (norm= 8-10mEq/L)
Calculating the anion gap
(Na+ + K+) - (Cl + HCO-3 bicarb)= anion gap
-Initial presents of type 1 DM
-Insufficient insulin relative to need
* Severe stress- trauma, surgery & acute MI
- Missed or reduced insulin
-Pregnancy in type 1 DM
- Medications: glucocorticoids (prednisone, etc)
- Mismanagement of sick days
DKA: Clinical presentation
- 3 P's (poly- uria, dipsia, phagia)
- Hyperventilation/Kussmaul's respirations
- Fruity odor breath / Acetone
- Flushed dry skin
- Lethargy/ altered consciousness
- Abd pain/NV
- Blood glucose ↑250 (much greater)
- metabolic acidosis
- Weight loss (may be profuound
Mainly type II DM
Elerdly w/decreased compensatory mechanisms to maintain homeostasis
Blood glucose >than DKA average 1000mg/dL
More electrolyte imbalances & renal dysfunction
Absent deep tendon reflexes, paresis & Babinski's sign
HHS: Medications that affect glucose levels
- Thiazide diuretics
- Phenytoin (Dilantin)- anticonvulsant
- Calcium channel blockers
- Enteral & parenteral nutrition
HHS vs. DKA
Blood sugar greater, average 1000mg/dL
More "normal" ABG's
More electrolyte imbalances
Higher serum osmolarity
DKA & HHS interventions
- Manage airway
- Fluid replacement 1st- 0.9% NS, then 0.45% NS
- Dextrose added when glucose approaches 200mg/dL
- Monitor closely for signs of fluid volume overload & cerebral edema
DKA & HHS: Dropping blood glucose
Drop slowly 50-75/hr
What is the key electrolyte to watch for in DKA & HHS?
Potassium. Osmotic diuresis results in total body k+ depletion ranging from 400-600mEq.
* k+ may be greater in HHS
Hyperglycemic: cause & trauma
- Blood clots
- Damage to vascular system
- On alert for drugs that ↑ BG (steroids)
Rapid acting insulin's:
Humalog (lispro), Novalog (aspart), Apidra (glulisine)
Onset: 15 mins
Novalog & Apidra's peak time is__________ & duration time is ___ to ___ hrs.
60-90min / 3 to 4 hrs
Insulin: Short acting
Regular (Humalin R, Novolin R, ReliOn R)
Onset: 1/2hr (30min)
Humalin R, Novolin R, and ReliOn R have a peak time of ______ & a duration time of ___hrs.
2-3hrs / 3-6hrs
Insulin: Intermediate acting
NPH (Humulin N, Novolin N, Relion N
Insulin: Long acting
Lantus (glargine) Levemir (detemir)
Onset: 1-2 hrs
Peak: NONE- NO PEAK
Which insulin has a duration time of a full day?
Lantus & Levemir (Long acting)
NPH (Humulin N, Novolin N, Relion N have a peak time of ______ & duration time of _____hrs.
4-10hrs / 10-16hrs
Transition from IV insulin to SQ
- Blood glucose is 200mg/dL or less & when 2 of the following have been met:
- Venous pH is ↑ 7.30
- Serum bicarb level is greater than 15mEq
- Calculated anion gap is 12 mEq or less
Weaning: Give SQ, then stop IV drip
Adrenal crisis: Primary
- Auto immune disease (Addisons < cortisol)
- Granulomatous: TB, sarcoidosis, histoplasmosis
- Hemorrhagic destruction- anticoag, trauma sepsis
- Infections: meningococcal, staph, pneumonia fungal, AIDS
- Drug: detoconazole, trimetroprim, etomidate, 5-fluorouracil (suppresses adrenals), rifampin
- Irradiation, adrenalectomy & genetic abnormality.
Adrenal crisis: Secondary
* Abrupt w/drawl of corticosteroids
* Pituitary - tumors, hemorrhage, radiation, cx
* Systemic inflammation: sepsis, vasculitis, sickle cell anemia
* Trauma- especially head trauma or surgery
* Hypothalamic DO's
Manifestations of adrenal insufficiency (AI) result from
Lack of adrenal cortical secretion of glucocosteroids primarily cortisol, mineralocorticoids primarily aldosterone or both.
* Most common cause is abrupt w/drawl of corticosteroids therapy
Longer acting agents such as ______________ are more likely to cause suppression than short acting corticosteroids like __________.
Dexamethasone / hydrocortisone
AI Laboratory values:
↓ Na+, blood glucose
↑ Ka+, Ca+
* Cortisol levels
* ACTH levels
*Cosyntropin stimulation test
* Symptoms of hypovolemia
* Fluid / electrolyte imbalances
~Postural hypotension, change LOC, ↑k+
* Fatigue & weakness
* GI complaints
* decreased renal perfusion & ↓ urine output
- Correct fluid / electrolyte imbalances- NS & dextrose. May need 5L in first 24 hrs.
- Hormonal replacement- Hydrocortisone (gluco) & Fludrocortisone (mineral)
- Patient and family education
Over production of thyroid hormone
Occurs in mismanagement of pt.'s w/hyperthyroidism
Medical emergency, death w/in 48hrs
Graves' disease (auto immune) most common cause
Thyroid storm Precipitating factors:
- General anesthesia
Thyroid storm: Presentation
↑ HR, palpitations- presents as sinus tachycardia when pt. is sleeping or A.Fib w/ventricular response.
↑ Irritable, hyper nervous
↑ Temperature, hot w/excessive sweating
↑ Appetite, stools & weight loss
↑ tremors of the tongue & eyelids- muscle wasting and tremors w/ activity
Skin: Thin, fine, fragile hair, soft nails, petechial. * Men ↑ acne & sweating
Eyes: Bulging out (exophthalmos), sight loss, lid lag (delayed movement of eye), Graefe's sign or Ptosis- drooping of upper or lower eyelid.
Thyroid storm: Medications/interventions
- Propylthiouracil (PTU) & methimazole (Tapazole)- they inhibit thyroid synthesis.
- Iodide agents- retard release of hormones
- Medication to block effects: beta-blockers, steroids
Primary- Hashimoto's or surgical or radioactive tx for Graves' disease
Secondary- Insufficient thyroid stimulation due to hypothalamus or pituitary disease
Most extreme form of hypothyroidism
Mostly common in elderly women- rare in young persons
Occurs more frequently in winter, due to ↑ stress to exposure to cold
Myexedema: Precipitating factors
- Trauma & critical illness
- Cognitive changes- everything slows down.
- Activity intolerance- decreased reflexes & slow movements
- Cardiovascular: bradycardia, hypotension, cardiomegaly
- ↓ cardiac output
- Hypoventilation, CO2 retention, pleural effusion
- Upper airway & tongue edema
Myexedema diagnoses: Primary
↓T3 and T4; T3 resin update with ↑ TSH
Hyponatremia ↓Na+- secondary to fluid retention
Myexedema diagnoses: Secondary
↓ T3 and T4; ↓ T3 resin update with ↓TSH (all are low)
Hyponatremia ↓Na+: secondary to fluid retention
Treat w/replacement thyroid hormone
Fluid/electrolyte replacement; thyroid replacement usually corrects sodium
Monitor gas exchange & respiratory status
Monitor cardiovascular status
Protect from injury & infection
Educate patient & family
Diabetes Insipidus (DI)
Deficiency in synthesis or release of antidiuretic hormone (ADH)
Excessive water loss
Neurogenic (central) ADH deficiency- primary cause traumatic injury to posterior pituitary or hypothalamus from head injury or surgery.
Nephrogenic Kidneys insensitive to ADH- occurs in genetically predisposed persons, or CRD, drugs, or other conditions that produce permanent kidney damage.
DI: Neurogenic etiology
- Genetically predisposed- familial, auto immune
- Head trauma
- ↑ ICP- from meningitis
- Pituitary surgery
- Infections: meningitis, encephalitis, syphilis
- TB, sarcoidosis
- Tumors: pituitary, metastases to hypothalamus
DI: Neurogenic acuity
- Occurs abruptly with onset of polyuria, as much as 5-40L in 24hrs
- Urine is pale & dilute, polydipsia, hypotension, ↓ skin turgor, dry mucous membranes, tachycardia, weight loss,
- Neuro signs are seen with hypovolemia & hypernatremia (↑Na+)
DI: Nephrogenic Etiology
- Genetically predisposed
- Chronic renal disease
- Multisystem disorder affecting kidney
- Metabolic disturbances: chronic ↓Ka+ and ↑Ca+
- Drugs: ethanol, phenytoin (Dilantin), Lithium carbonate, demeclocycline, Amphotericin, Methoxyflurane (inhaled anesthetic)
↑ urine output
Thirst & polydipsia
↓ skin turgor
Dry mucous membranes
Neuro changes w/: hypernatremia & hypovolemia
DI: Labs for diagnosis
UA- dilute urine w/low specific gravity
↑ serum osmolarity
↑ BUN / Creatinine
Hypokalemia & hyperkalemia
Water deprivation test
Vasopressin test to differentiate
DI lab indicators:
Sodium (serum) >145mEq/L
Osmolality (serum) > 295 mOsm/kg H20
Osmolality (urine) <100 mOsm/kg H20
Sodium (urine) 40-200mEq/L = Not affected
- Volume replacement- monitor for fluid overload & water intoxication.
- Hormone replacement- vasopressin (desmopressin)
- Thiazide diuretics (nephrogenic)- monitor neuro status, fluid status, electrolyte status or both.
exact opposite of diabetes insipidous
- Excess ADH
- Plasma hypotonicity
Central Nervous System disease
- Small-cell lung carcinoma
- Hodgkin's lymphoma
- Pancreatic & duodenal carcinoma
- TB, lung abscess, pneumonia, COPD
- Many medications can result in SIADH
- ↑ respirations, dyspnea & adventitious lung sounds
- ↑ Central venous pressure (CVP) & PA pressure (pulmonary artery)
- Anorexia, NV, muscle cramps & ↓ bowel sounds
Decreased serum osmolality
High urine sodium
Decreased BUN (normal 7-20mg/dL) & Creatinine
- Fluid restriction 800-1000ml/day
- If needed hypertonic saline & diuretics
- I&O's, serum sodium, urine & serum specific gravity and daily weights
- Loop diuretics
- Mouth / skin care
- Patient & family education
SIADH: lab indicators
Sodium (serum) <135 mEq/L
Osmolality (serum) <280 mOsm/kg H20
Osmolality (urine) > 100 mOsm/kg H20
Sodium (urine) > 200 mEq/L
Cerebral Salt Wasting (CSW)
Result of serious brain injury
Disorder of sodium or fluid balance
Similar to SIADH
Patho is not understood
- defect in sodium transport
- Weight loss
- Dry mucous membranes; poor skin turgor
- Lethargy & weakness
- Mental status changes
- Seizure & coma
CSW: Lab indicators
Sodium (serum) <135 mEq/L
Osmolality (serum) <295 mOsm/kg H20
Osmolality (urine) < 100 mOsm/kg H20
Sodium (urine) > 200 mEq/L
- Restore sodium & fluid volume
- Isotonic Saline
- Hypertonic saline
II. Oral or IV fludrocortisone
Cranial nerve IV:
Oculocephalic response, a neurop reflex that determines brain stem activity.
* Hold eyes open & turn head side to side- If eyes move bilaterally in opposite direction of head movement= means doll's eye reflex is present & cranial nerve is intact.
They can still hear!
You can tell they are stressed or emotional by their VS. ↑VS not good for ICP or stroke pt.
Drug of choice for brain & spine injury
Decadon (dexamethasone), & methylpredisone (solumedrol) for spine & brain injury
Criteria for rtPa
Less than 3hrs since injury
Ischemic stroke only
No open wounds
> 18yrs of age
SCI: Complete lesion
Total loss of motor, sensory & reflex activity from waist down
SCI: Central cord syndrome
Hip to Lower neck- loss of motor function in upper shoulders
ABD- incomplete loss of motor function
Brown Sequard syndrome:
Loss of pain, temperature & light touch on opposite side of injury
Loss of motor function, vibration, position & deep touch sensation on same side as cord damage.
*Opposite side to injury site you lose sensation & on same side of injury site you lose motor function.
Lab values: AST
*In elderly slightly higher
* Females slightly lower
Lab values: ALT
4-36 international units/L
* Men, elderly & African Americans are slightly higher
↓ 7.35 is acidic
↑ 45 is acidic
↓ metabolic acidosis
Kidneys will retain increases amounts of HCO-3 to ↑ pH
* opposite for alkalosis
Lungs "blow off" CO2 to raise pH
* opposite for alkalosis