Critical care exam II notes
BUN
10-20 mg/dL
Creatinine:
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)
MAP-ICP= CPP
Cerebral perfusion
Optimal cerebral perfusion:
>13 on Glasgow coma scale
<4 NIHSS
<20 ICPmm/Hg
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
70mm/Hg
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
Battle sign
Bilateral periorbital edema & bruising, and otorrhea.
Raccoon's eyes
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
ICP: Symptoms
Early= HTN
Late= Cushing's triad- irreversible
Cushing's triad consists of HTN, w/widening pulse pressure, bradycardia & irregular respirations--> Irreversible
ICP: Interventions
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.
Cerebral oxygenation:
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.
Recommended PbtO2
20mm/Hg or device specific
- ABG's
- SpO2
- 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.
Stroke assessment:
- Eval mental status (LOC arousal, oritentation)
- Cranial nerve function motor strength, sensory function, nerve function
- Motor strength
- Sensory function
- Coordination
- Deep tendon reflexes
NIHSS is use:
To assess severity of presenting signs/symptoms, especially if pt.'s is a candidate for a thrombolytic therapy.
Stroke signs/symptoms:
* 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"
Stroke monitoring:
- 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 _____.
airway
C1-C3 injury
ventilator dependency
C4-C5 injury
Phrenic nerve impairment, tx w/phrenic nerve pacemaker.
* VERY IMPORTANT FOR BREATHING!
C5-T6
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
SCI alignment:
To prevent further trauma use 3 people to turn and stabilize head and neck when moving them.
SCI: GI
Can develop fecal impaction, monitor for BM and supply daily stool softener.
Spinal shock:
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
Neurogenic shock:
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:
- Hypotension
- Bradycardia- may be sever enough for a temp pacemaker
- Hypothermia
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!
Hypotension
Neuro type pt.'s get ____ instead of saline bolus.
albumin
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
Depresses seizure
- 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°
Seizure Interventions:
- 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
Dilantin level/range:
Therapeutic Range:: Total: 10 to 20 mcg/ml.
Toxic level: >20-30 mcg/ml
1st choice medication for seizures:
Ativan IV
*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
(AD) Interventions:
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:
Droplet precautions
Assess for fever, cough
Dim light
Private room
Have visitors put on PPE
Mannitol or hypertonic saline given
Ventriculostomy catheter to drain CSF
ABX ASAP
↑ HOB 30-40°
IV corticosteroids
Clinical manifestations of Bacterial meningitis:
- HA
- Fever
- Vomiting
- Rash
- 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
flexed.
Bacterial meningitis:
Neurological emergency
- infection of the pia & arachnoid layers
- CSF
Hypoglycemic episode:
Glucose <70 mg/dL
AKA insulin shock or Insulin reaction
1st clinical sign- ↓mental status change
Hypoglycemia: Rapid
ANS stimulations: Activates SNS-> release of epinephrine
- Nervousness, apprehension, tremors
- Tachycardia, palpitations, tremors
- Pallor
- Diaphoretic
- Dilated pupils
- Fatigue & weakness
- HA
- Hunger
Hypoglycemia: Prolonged
- Headache
- Restlessness
- Difficulty speaking/thinking
- Difficulty walking
- Visual disturbances (double vision, field deficit
- Paresthia
- 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
DKA:
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
DKA: Etiology
-Initial presents of type 1 DM
-Infections
-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
- Orthostasis
- 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)
- Ketonuria/glucosuria
- metabolic acidosis
- Weight loss (may be profuound
HHS:
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
Profound dehydration
Stress response
HHS: Medications that affect glucose levels
- Thiazide diuretics
- Phenytoin (Dilantin)- anticonvulsant
- Glucocorticoids
- Beta-blockers
- 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
No ketones!
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
- Infection
- 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
Peak: 60-90mins
Duration: 3-4hrs
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)
Peak: 2-3hrs
Duration: 3-6hrs
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
Onset: 2-4hrs
Peak: 4-10hrs
Duration: 10-16hrs
Insulin: Long acting
Lantus (glargine) Levemir (detemir)
Onset: 1-2 hrs
Peak: NONE- NO PEAK
Duration: 24°
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+
Metabolic acidosis
Eosinophilia
Hyperuricemia
* Cortisol levels
* ACTH levels
*Cosyntropin stimulation test
AI Assessment:
* Symptoms of hypovolemia
* Fluid / electrolyte imbalances
~Postural hypotension, change LOC, ↑k+
* Fatigue & weakness
* GI complaints
* decreased renal perfusion & ↓ urine output
AI interventions
- Correct fluid / electrolyte imbalances- NS & dextrose. May need 5L in first 24 hrs.
- Hormonal replacement- Hydrocortisone (gluco) & Fludrocortisone (mineral)
- Patient and family education
Thyroid Storm:
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:
- Stress
- General anesthesia
- Surgery
- Infection
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
Myexedema
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
Life threatening
Mostly common in elderly women- rare in young persons
Occurs more frequently in winter, due to ↑ stress to exposure to cold
Myexedema: Precipitating factors
- Hyperthermia
- Infection
- Stroke
- Trauma & critical illness
Myexedema: Assessment
- Cognitive changes- everything slows down.
- Activity intolerance- decreased reflexes & slow movements
- Cardiovascular: bradycardia, hypotension, cardiomegaly
- ↓ cardiac output
- Edema
- Hypoventilation, CO2 retention, pleural effusion
- Upper airway & tongue edema
- Hypothermia
Myexedema diagnoses: Primary
↓T3 and T4; T3 resin update with ↑ TSH
Hypoglycemia
Hyponatremia ↓Na+- secondary to fluid retention
Myexedema diagnoses: Secondary
↓ T3 and T4; ↓ T3 resin update with ↓TSH (all are low)
Hypoglycemia
Hyponatremia ↓Na+: secondary to fluid retention
Myexedema interventions:
Treat w/replacement thyroid hormone
Fluid/electrolyte replacement; thyroid replacement usually corrects sodium
Monitor gas exchange & respiratory status
Monitor cardiovascular status
Manage hypothermia
Protect from injury & infection
Educate patient & family
Diabetes Insipidus (DI)
Deficiency in synthesis or release of antidiuretic hormone (ADH)
Excessive water loss
Types:
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)
DI: Assessment
↑ urine output
Thirst & polydipsia
Hypotension
↓ skin turgor
Dry mucous membranes
Tachycardia
Weight loss
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
DI intervention:
- Volume replacement- monitor for fluid overload & water intoxication.
- Hormone replacement- vasopressin (desmopressin)
- Thiazide diuretics (nephrogenic)- monitor neuro status, fluid status, electrolyte status or both.
SIADH:
exact opposite of diabetes insipidous
- Excess ADH
- Plasma hypotonicity
SIADH: Etiology
Central Nervous System disease
- Trauma
- Tumor
Malignancy
- Small-cell lung carcinoma
- Hodgkin's lymphoma
- Pancreatic & duodenal carcinoma
Pulmonary disorders
- TB, lung abscess, pneumonia, COPD
Medications
- Many medications can result in SIADH
SIADH: Assessment
CNS:
- Confusion
- HA
- Seizures
- Weakness
Pulmonary
- ↑ respirations, dyspnea & adventitious lung sounds
Cardiovascular
- HTN
- ↑ Central venous pressure (CVP) & PA pressure (pulmonary artery)
GI system
- Anorexia, NV, muscle cramps & ↓ bowel sounds
SIADH: Diagnosis
Hyponatremia
Decreased serum osmolality
High urine sodium
Concentrated urine
Decreased BUN (normal 7-20mg/dL) & Creatinine
Decreased albumin
SIADH: interventions
- 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
CSW Assessment
- Tachycardia
- Weight loss
- Hypotension
- 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
CSW: interventions
- Restore sodium & fluid volume
- Isotonic Saline
- Hypertonic saline
II. Oral or IV fludrocortisone
Dolls eyes
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.
Comatose patient
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
Not pregnant
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
0-35 units/L
*In elderly slightly higher
* Females slightly lower
Lab values: ALT
4-36 international units/L
* Men, elderly & African Americans are slightly higher
pH:
7.35-7.45
↓ 7.35 is acidic
Pco2: Respiratory
35-45
↑ 45 is acidic
HCO-3:
22-26
↓ metabolic acidosis
Respiratory acidosis
Kidneys will retain increases amounts of HCO-3 to ↑ pH
* opposite for alkalosis
Metabolic acidosis
Lungs "blow off" CO2 to raise pH
* opposite for alkalosis