10-20 mg/dL

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

13-15 is a good score to have.

<8 coma!!! ;(

MAP-ICP= CPP

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

< 20 mmg/Hg

70mm/Hg

* Still worry about the airway & breathing

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.

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)

Battle sign

Raccoon's eyes

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

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

Early= HTN

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

Diagnostic testing for ICP & TBI

Radiological studies/diagnostic test ICP

Evoked potential monitoring

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

- Coordination

- Deep tendon reflexes

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.

Head in proper alignment, collar placed.

airway

ventilator dependency

Phrenic nerve impairment, tx w/phrenic nerve pacemaker.

* VERY IMPORTANT FOR BREATHING!

Intact diaphragmatic breathing, w/varying impairment of intercostal and abdominal muscle function.

* 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:

1. Hypotension
2. Bradycardia- may be sever enough for a temp pacemaker
3. Hypothermia

Duration varies & resolution is signaled by return of sympathetic tone

Mannitol- It is osmotic, pulls water from brain interstitium into plasma.

* Used to treat ICP

* Use inline filter to administer & check for crystals.

Hypotension

albumin

Why? Albumin is a volume extender.

BP is more important than temperature- only if abnormal

Depresses seizure

• Use separate line
• Mixed w/NS only

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!!

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

Ativan IV

*If it fails to stop seizure in 10mins or if intermittent seizure persists longer than 20mins try-> Phenytoin (Dilantin) or fosphenytoin (Cerebyx)

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

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

1. HA
2. Fever
3. Vomiting
4. Rash
5. 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.

Neurological emergency

• infection of the pia & arachnoid layers
• CSF

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
• Pallor
• Diaphoretic
• Dilated pupils
• Fatigue & weakness
• HA
• Hunger

• 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)

• 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)

(Na+ + K+) - (Cl + HCO-3 bicarb)= anion gap

-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

• 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

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

1. Thiazide diuretics
2. Phenytoin (Dilantin)- anticonvulsant
3. Glucocorticoids
4. Beta-blockers
5. Calcium channel blockers
6. Enteral & parenteral nutrition

Blood sugar greater, average 1000mg/dL

More "normal" ABG's

More electrolyte imbalances

Higher serum osmolarity

No ketones!

1. Manage airway
2. Fluid replacement 1st- 0.9% NS, then 0.45% NS
3. Dextrose added when glucose approaches 200mg/dL
4. Monitor closely for signs of fluid volume overload & cerebral edema

Drop slowly 50-75/hr

Potassium. Osmotic diuresis results in total body k+ depletion ranging from 400-600mEq.

* k+ may be greater in HHS

• Infection
• Blood clots
• Damage to vascular system
• On alert for drugs that ↑ BG (steroids)

Onset: 15 mins

Peak: 60-90mins

Duration: 3-4hrs

60-90min / 3 to 4 hrs

Onset: 1/2hr (30min)

Peak: 2-3hrs

Duration: 3-6hrs

2-3hrs / 3-6hrs

Onset: 2-4hrs

Peak: 4-10hrs

Duration: 10-16hrs

Onset: 1-2 hrs

Peak: NONE- NO PEAK

Duration: 24°

Lantus & Levemir (Long acting)

4-10hrs / 10-16hrs

- Blood glucose is 200mg/dL or less & when 2 of the following have been met:

1. Venous pH is ↑ 7.30
2. Serum bicarb level is greater than 15mEq
3. Calculated anion gap is 12 mEq or less

Weaning: Give SQ, then stop IV drip

- 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.

* 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

Lack of adrenal cortical secretion of glucocosteroids primarily cortisol, mineralocorticoids primarily aldosterone or both.

* Most common cause is abrupt w/drawl of corticosteroids therapy

Dexamethasone / hydrocortisone

↓ Na+, blood glucose

↑ Ka+, Ca+

Metabolic acidosis

Eosinophilia

Hyperuricemia

* 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

1. Correct fluid / electrolyte imbalances- NS & dextrose. May need 5L in first 24 hrs.
2. Hormonal replacement- Hydrocortisone (gluco) & Fludrocortisone (mineral)
3. 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

1. Stress
2. General anesthesia
3. Surgery
4. Infection

↑ 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.

• 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

Life threatening

Mostly common in elderly women- rare in young persons

Occurs more frequently in winter, due to ↑ stress to exposure to cold

• Hyperthermia
• Infection
• Stroke
• Trauma & critical illness

• 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

↓T3 and T4; T3 resin update with ↑ TSH

Hypoglycemia

Hyponatremia ↓Na+- secondary to fluid retention

↓ T3 and T4; ↓ T3 resin update with ↓TSH (all are low)

Hypoglycemia

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

Manage hypothermia

Protect from injury & infection

Educate patient & family

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.

• Genetically predisposed- familial, auto immune
• Head trauma
• ↑ ICP- from meningitis
• Pituitary surgery
• Infections: meningitis, encephalitis, syphilis
• TB, sarcoidosis
• Tumors: pituitary, metastases to hypothalamus

• 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+)

1. Genetically predisposed
2. Chronic renal disease
3. Multisystem disorder affecting kidney
4. Metabolic disturbances: chronic ↓Ka+ and ↑Ca+
5. Drugs: ethanol, phenytoin (Dilantin), Lithium carbonate, demeclocycline, Amphotericin, Methoxyflurane (inhaled anesthetic)

↑ urine output

Thirst & polydipsia

Hypotension

↓ skin turgor

Dry mucous membranes

Tachycardia

Weight loss

Neuro changes w/: hypernatremia & hypovolemia

UA- dilute urine w/low specific gravity

↑ serum osmolarity

↑ BUN / Creatinine

Hypokalemia & hyperkalemia

Water deprivation test

Vasopressin test to differentiate

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.

• Excess ADH
• Plasma hypotonicity

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

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

Hyponatremia

Decreased serum osmolality

High urine sodium

Concentrated urine

Decreased BUN (normal 7-20mg/dL) & Creatinine

Decreased albumin

• 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

Sodium (serum) <135 mEq/L

Osmolality (serum) <280 mOsm/kg H20

Osmolality (urine) > 100 mOsm/kg H20

Sodium (urine) > 200 mEq/L

Result of serious brain injury

Disorder of sodium or fluid balance

Similar to SIADH

Patho is not understood

• defect in sodium transport

• Tachycardia
• Weight loss
• Hypotension
• Dry mucous membranes; poor skin turgor
• Lethargy & weakness
• Mental status changes
• Seizure & coma

Sodium (serum) <135 mEq/L

Osmolality (serum) <295 mOsm/kg H20

Osmolality (urine) < 100 mOsm/kg H20

Sodium (urine) > 200 mEq/L

1. 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.

Decadon (dexamethasone), & methylpredisone (solumedrol) for spine & brain injury

Less than 3hrs since injury

Ischemic stroke only

Not pregnant

No open wounds

> 18yrs of age

Total loss of motor, sensory & reflex activity from waist down

Hip to Lower neck- loss of motor function in upper shoulders

ABD- incomplete loss of motor function

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.

0-35 units/L

*In elderly slightly higher

* Females slightly lower

4-36 international units/L

* Men, elderly & African Americans are slightly higher

7.35-7.45

↓ 7.35 is acidic

35-45

↑ 45 is acidic

22-26

↓ 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