Advanced Medical Life Support

Chapter 7

Altered Mental Status

Topics
Terminology and Altered Mental Status
Pathophysiology of Altered Mental Status General Assessment and Management of Altered Mental Status Differential Diagnosis: Intracranial Causes of Altered Mental Status Differential Diagnosis: Extracranial Causes of Altered Mental Status

7-2

C ASE S TUDY
Situation
Early in your shift, you respond to the residence of a male patient with altered mental status. On arrival, you are greeted by anxious family members who inform you that the patient is in an upstairs bedroom.

7-3

C ASE S TUDY
Situation
History & Findings
While evaluating the scene for hazards, you make your way to the bedroom and find the patient supine on the bed, making loud gurgling noises. As you pass a nightstand, you note cigarettefilled ashtrays and medicine containers labeled Lovastatin and Vasotec.
7-4

Terminology & Altered Mental Status

Altered mental status pertains to any decline in a patients responsiveness or behavior. Changes can be subtle and varied, but accurate documentation is absolutely essential to good care.

7-5

Commonly Used Terminology

Amnesic state

Coma Confusion

Decreased LOC

Amnesia is the loss of memory, the inability to recall past events. Described as retrograde (prior to an event), antegrade (after an event) or general not pertaining to an event) function. An absolute state of unresponsiveness. An individual who exhibits a relative level of consciousness but is disturbed in the perception or remembrance of person, place, time or events is said to be suffering confusion. Applies to any state in which the patient presents as anything other than alert with full orientation and normal cognition.
(continued)
7-6

Commonly Used Terminology

Delirium

Lethargy

Stupor

A state of confusion that is accompanied by auditory or visual hallucinations and/or incoherent or irrelevant speech. The patient may exhibit a normal-to-decreased level of consciousness. Pertains to a normal-to-decreased level of consciousness associated with the inability to react or respond to stimuli with normal perception or speed. Also describes a condition of drowsiness or indifference. An unresponsive state from which the patient can be transiently aroused by means of external stimuli. When the stimulus ceases, the patient returns to unresponsiveness.
7-7

Important to Note...
An exact description of altered mental status is clinically important and must be conveyed without any room for misinterpretation.

7-8

Pathophysiology
Consciousness, or the ability to perceive ourselves and the environment in which we exist, is a direct function of the cerebrum and the reticular activating system (RAS).

7-9

The Cerebrum
(Left hemisphere)
General sensory area

Sensory assoc. area

Parietal lobe Occipital lobe Visual assoc. area

Premotor area
Motor area

Frontal lobe
Motor speech area Temporal lobe

Visual area
Auditory area

Auditory assoc. area

7-10

Structural & Metabolic Alterations

Structural (areas of physical damage)
Brain tumor Stroke Encephalitis

Metabolic (originate outside the CNS)

Hypoxia Hypoglycemia Electrolyte imbalance
7-11

Regions of the Brain

Thalamus
Hypothalamus Cerebrum

2 Cerebral hemispheres

DIENCEPHALON

Midbrain Pons

Cerebellum

BRAINSTEM Medulla
oblongata
7-12

General Assessment & Management

Scene Size-up
Ensure scene safety. Seek clues in the immediate environment.

Initial Assessment
General impression. Chief complaint. Baseline mental status. ABCs. Patient priority.
7-13

General Assessment & Management (continued)

Focused History & Physical Exam
Physical exam Further mental status assessment Vital signs History

Adjunctive Equipment & Interventions Ongoing Assessment

7-14

Scene Size-Up
Characteristics of scene

Safety hazards
Scope of situation
Warning: any condition that alters mental status can alter a patients perception, resulting in violent behavior.
7-15

Initial Assessment
General Impression: When approaching,
establish an initial impression.

Chief Complaint: Determine the chief complaint,

which will be a major clue to the underlying cause of altered mental status.

Baseline Mental Status: Quickly establish an

initial level of consciousness.

The ABCs: Assess airway, breathing and

circulation.
7-16

Assess Mental Status

Upon reaching the patients side, quickly establish an initial level of consciousness. AVPU is a widely accepted method for accomplishing this task.

AVPU Assessment of Mental Status

A V P U Patient is ALERT Patient responds to VERBAL stimuli Patient responds to PAINFUL stimuli Patient is UNRESPONSIVE
7-17

Assess the Airway

Patient alert, conversing normally?
(Airway probably OK; check breathing.)

Mentation compromised?
(Airway suspect until proven otherwise.)
Check for secretions, substances & obstructions; suction as necessary. Try inserting an oral airway. If patient tolerates that, proceed to advanced airway control.

Caution: Watch & listen to breathing!

7-18

Assess Breathing
Adequate respiratory rate?
(Should be 8-24 breaths/min.)

Regular rhythm?
Adequate tidal volume?
(Look, listen, feel.)
LOOK for normal chest rise LISTEN & FEEL for air movement

7-19

Assess Breathing
Abnormal Respiratory Patterns
Name
Kussmauls
(acidosis)

Pattern

Description
Very deep. May be rapid, normal, or slow. Pattern of crescendo, decrescendo, apnea No coordinated pattern Long, deep breaths separated by apnea
7-20

Central neurogenic
(brain injury/herniation)

Cheyne-Stokes
(metabolic disease; stroke)

Biots, also called ataxic

(stroke)

Apneustic
(severe CNS disease/stroke)

Assess the Circulation

Pulse
Rate Strength Regularity

Peripheral perfusion
Skin color, temp & condition Capillary refill

7-21

Important to Note...
Patients with altered mental status always warrant consideration of prompt transport.

7-22

Focused History & Physical

Gather a history. Perform a physical exam. Assess baseline vital signs.
Order Varies Based on Patients Mental Status:
Responsive
1. History 2. Focused medical assessment 3. Baseline vital signs

Altered / Unresponsive
1. Rapid medical assessment 2. Baseline vital signs 3. History
7-23

Focused History & Physical

Further Mental Status Assessment
Glasgow Coma Scale
Eye Opening Spontaneous To Voice To Pain None Verbal Response Oriented Confused Inappropriate Words Incomprehensible Words None Motor Response Obeys Commands Localizes Pain Withdraw (Pain) Flexion (Pain) Extension (Pain) None Glasgow Coma Score Total 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1

Responsive

Unresponsive

7-24

Focused History & Physical

History

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Sx surrounding altered mentation may help to isolate the cause, i.e.:

Pathological breathing pattern Decorticate/decerebrate posturing Facial droop Ataxia Hyperactivity Neck pain/rigidity Others...
7-25

Focused History & Physical

History (continued)

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Helps to prevent the possibility of administering medications patients may be allergic to, and may yield clues as to the cause of altered mental status.

7-26

Focused History & Physical

History (continued)

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

May provide insight into patients past medical history; may suggest a cause of altered mentation.

Examples include insulin, antihypertensives, thyroid medications & nitroglycerin.

7-27

Focused History & Physical

History (continued)

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

May suggest exacerbation of pre-existing problem as cause of present change in mentation. Examples include previous stroke, hypertension and use of alcohol or other drugs.
7-28

Focused History & Physical

History (continued)

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Can be important in the insulin-dependent diabetic who has not eaten. Since many electrolytes and vitamins are obtained via diet, this may impact electrolyte balance.
7-29

Focused History & Physical

History (continued)

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Behavior or complaints surrounding onset of abnormal behavior can be help to isolate the cause of altered mentation. Examples include trauma especially head trauma), exertion, rest, and seizures.
7-30

Adjuncts & Interventions

Adjunctive Equipment

Cardiac monitor
Pulse oximeter

Glucometer (or reagent stick)

Evaluate blood glucose level of anyone who exhibits a change in mental status. < 40 mg/dl may indicate hypoglycemia. More than 300 mg/dl may indicate hyperglycemia.
7-31

Important to Note...
In cases of hypoventilation or noted hypoxia, the use of pulse oximetry must not delay the application and delivery of much-needed oxygen.

7-32

Adjuncts & Interventions

Interventions to be Considered

Intravenous access
Drawing of blood specimens

Fluid therapy
Endotracheal intubation

7-33

Ongoing Assessment
Repeat initial assessment.
(including evaluation of mental status)

Reassess vital signs.

Repeat physical exam.

Check interventions.

7-34

Differential Diagnosis
Intracranial Causes: Head Injuries

Types of Injuries
Cerebral concussion Cerebral contusion Epidural hematoma Subdural hematoma Intracerebral hemorrhage
7-35

Cranial Anatomy
The Meninges of the Brain
Dura mater Pia mater Arachnoid membrane

Cranium

Dura mater Arachnoid membrane Pia mater

Cranium Brain

Foramen magnum Spinal cord

7-36

Differential Diagnosis
Intracranial Causes: Stroke

Often called a cerebral vascular accident (CVA) or brain attack.

Produces disruption of blood supply to brain tissue. Progresses from ischemia to infarction. Classified as either occlusive or hemorrhagic.

7-37

Differential Diagnosis
Intracranial Causes: Stroke (continued)

Occlusive Stroke
Thrombotic stroke
- Localized thrombus (blood clot) - Plaque deposits narrow lumen of cerebral artery - History of gradual progression of mental/neurologic changes - Patient commonly awakens with stroke findings

Embolic stroke

- Embolus breaks free from remote site and occludes artery - Onset is abrupt & without warning signs - Physical exertion often surrounds onset

7-38

Causes of Occlusive Stroke

Atherosclerotic Disease

Atherosclerosis is primary cause

Contributing factors: Hypercholesteremia

Diabetes mellitus Genetics Obesity Physical inactivity
Oral contraceptives and cigarette smoking can predispose individuals to thrombus and embolus formation.
7-39

Differential Diagnosis
Intracranial Causes: Stroke (continued)

Transient Ischemic Attack (TIA)

May be a thrombotic or embolic occlusion Signs and symptoms are transient Body is able to dissolve the occlusion One-third of TIA sufferers eventually also experience a serious stroke

7-40

Differential Diagnosis
Intracranial Causes: Stroke (continued)

Hemorrhagic Stroke
Occurs secondary to rupture of cerebral artery
- Brain cells become ischemic and eventually infarct

- Blood from rupture accumulates to form intracranial hematoma

Hypertension is primary cause

Occurs most often when BP is high Onset abrupt & severe, with rapid decline in mental status Severe headache common just prior to stroke

7-41

Assessment of Stroke or TIA

Thorough Scene Size-Up
Insulin containers, other medications Home oxygen Glucometers

Initial Assessment
Suspect patients inability to clear secretions Decorticate or decerebrate posturing
7-42

Neurologic Exam
Tests of Cranial Nerve Function

Check for...
Visual disturbances Pupillary size, equality & response Facial droop Swallowing difficulty Tongue deviation

To assess function of...

Optic nerve/II cranial nerve Oculomotor nerve/III cranial nerve Facial nerve/VII cranial nerve Glossopharyngeal nerve/IX cranial nerve Hypoglossal nerve/XII cranial nerve

Other Neurologic Function Tests

Check for...
Motor function (grip) Sensory ability in the extremities Strength in the extremities Gait ataxia Incontinence
7-43

Signs of Advanced Brain Injury

Posturing

Decorticate

Decerebrate

7-44

Assessment of Stroke or TIA

Focused History

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

The following list warrants special attention:

Headache Declining / improving mental or neuro status Hemiplegia Hemiparesis Dysphasia or aphasia Cardiac symptoms Nausea or vomiting Syncopal episodes

7-45

Assessment of Stroke or TIA

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Note & relay patient allergies.

7-46

Assessment of Stroke or TIA

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Pay special attention to information about:

Anticoagulants/antiplatelet agents (ASA, Coumadin) Antihypertensives Anticholesteremics Cardiac meds Insulin/antihyperglycemics Oral contraceptives
7-47

Assessment of Stroke or TIA

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Is the patient predisposed to stroke? Yes, if Hx reveals:

Previous stroke or TIA Previous head trauma Hypertension Atherosclerosis or CAD Hypercholesteremia Cardiac arrhythmias Aneurysms or AV malforms Diabetes mellitus Cigarette smoking

7-48

Assessment of Stroke or TIA

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

May suggest possibility of vomiting & aspiration May be important if surgery is an issue

7-49

Assessment of Stroke or TIA

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Understanding the onset of a stroke is key to diagnosis -- especially:

Gradual vs. acute onset Time of onset Improving or declining mental or neurological status Complaints preceding incident Occurrence during rest, on exertion Associated seizure activity
7-50

Management of Stroke or TIA

Initial Priorities

Aggressive airway management Aggressive oxygenation

(consider hyperventilation!)

Hyperventilation excretes CO2 CO2 is a potent vasodilator Excretion of CO2 vasoconstriction, ICP

Rapid transport to appropriate facility

7-51

Important to Note...
Overzealous ventilation can prove detrimental to the patient.
Too much loss of CO2 can produce excessive cerebral vasoconstriction Cerebral perfusion may be decreased Titrate ventilations to maintain PaCO2 between 25-30 mmHg.
7-52

Management of Stroke or TIA

Other Therapies

Use IV isotonic crystalloids.

Maintain @ TKO rate to minimize ICP.
Avoid dextrose.
- Cerebral edema & poor neurological outcomes may result. - Sugar metabolism forces fluid shift from vessels to brain tissue.

7-53

Management of Stroke or TIA

Other Therapies (continued)
Consider treatment of persistent strokeinduced hypertension
If BP remains at 220/120 for 60-90 minutes For a hemorrhagic stroke, reduce BP to
prehemorrhagic levels Reducing hypertension serves to:
- Decrease size of bleed - Prevent further rupture - Deter rebleeding in clotted areas

7-54

Management of Stroke or TIA

Other Therapies (continued)
Can be complicated.

Vasodilators may increase ICP.

Beta-blockers may be helpful.

Drastic reduction of BP may impair cerebral perfusion, worsening ischemia & extending infarct.
7-55

Differential Diagnosis
Intracranial Causes: Cranial Infection
Pathogen infects the brain or supporting structures
Represents a structural alteration with consequent mental or behavioral changes Most common infectious processes: Meningitis Encephalitis Cerebral abscess
7-56

Cranial Infections
Meningitis
Infection & inflammation of meningeal membranes surrounding brain
May be caused by bacterium, virus or fungus Inflammation of meninges increases ICP Infection can spread to brain and cause cerebral abscess or encephalitis
7-57

Cranial Infections
Signs & Symptoms of Meningitis
Alterations in mental status may include: Drowsiness
Stupor Coma Seizures

Fever Nausea and/or extensive vomiting May complain of persistent headache

7-58

Cranial Infections
Signs & Symptoms of Meningitis (continued)
Nuchal rigidity Intolerance to light, sound or ocular motion Other signs suggesting inflammation
BRUDZINSKIs Sign: Flexion of head produces neck pain & reflexive flexion of hips & knees KERNIGs Sign: Flexion of extremities w/ pain & resistance on subsequent straightening HEMIPARESIS: One-sided paralysis FLACCIDITY: Loss or lack of muscle tone
7-59

Cranial Infections
Encephalitis
Infection of brain tissue
Most often viral

Generally results from an infection that occurred somewhere else in body

Inflammation & tissue destruction alter cerebral function
7-60

Cranial Infections
Signs & Symptoms of Encephalitis
Fever Headache Personality changes Confusion Progression involves: Agitation
Seizures Stupor Coma

7-61

Cranial Infections
Signs & Symptoms of Encephalitis (continued)
Depending on extent of infection, other neurologic deficits may also appear. Ataxia
Pupil irregularities It is difficult to distinguish encephalitis from Visual disturbances Facial or ocular palsies meningitis in the field. Nuchal rigidity
7-62

Cranial Infections
Cerebral Abscess
Localized accumulation of pus within the brain
Develops when residue from bacterial invasion liquefies and accumulates leukocytes, tissue debris and proteins Capsule forms around pus to contain byproducts

Often begins as infection of nasal cavity, middle ear or mastoid cells (can also occur from open skull fractures or intracranial operations)
7-63

Cranial Infections
Signs & Symptoms of Cerebral Abscess
Overt changes in mental status
Chronic headache that worsens Focal neurological deficits If abscess ruptures, meningitis or encephalitis may result

7-64

Assessment of Cranial Infections

Assessment of a cranial infection follows the same generic framework as that of any patient with altered mental status.

If infection is suspected, assessment should work toward describing where it has established itself in the brain and the severity to which it has progressed.
7-65

Management of Cranial Infections

Emotional support Subsidize decreased or lost vital functions Patent airway
High-flow O2 Manage increased ICP through hyperventilation IV of isotonic crystalloid (NS)
- Run TKO unless significantly dehydrated - If dehydrated, administer fluid boluses of 20 mL/kg (avoid fluid overload) - Draw blood for laboratory analysis

7-66

Differential Diagnosis
Intracranial Causes: Seizure Activity

Seizures can be idiopathic or can occur secondary to other disorders of the following types:
CNS injury / dysfunction Metabolic disturbance Infection
7-67

Differential Diagnosis
Intracranial Causes: Intracranial Tumor
A growing mass within the cranium, found within or on any cerebral structure
Tumor expands, increasing ICP Compression of tissue and cerebral vessels leads to damage and herniation

Patients mental status depends on tumors size, location and rate of growth
7-68

Intracranial Tumor
Common Complaints
Confusion
Amnesia Lethargy Sudden personality changes As ICP increases: Headache
Vomiting Seizure activity
7-69

Intracranial Tumor
Common Complaints (continued)
Depending on size and location, may produce focal neurologic deficits
If herniation ensues, a decrease in LOC will progress to stupor and/or coma

7-70

Assessment of Intracranial Tumor

Assessment of an intracranial tumor follows the same generic framework as that of any patient with altered mental status.
Since an intracranial tumor can cause cognitive and/or neurologic dysfunction, assessment closely parallels the assessment of stroke.
7-71

Management of Intracranial Tumor

Control of intracranial pressure Subsidize decreased or lost vital functions Ensure patent airway
High-flow oxygen Manage increased ICP (consider hyperventilation) IV isotonic crystalloid (e.g., 0.9% normal saline)

Manage seizure activity as indicated

7-72

Differential Diagnosis
Extracranial Causes: Pulmonary Disorders
Pulmonary system plays a direct role in brain function.
Brain activity is highly metabolic & dependent on oxygen. In response to hypoxia, brain cells resort to anaerobic metabolism to produce ATP. Long-term anaerobic metabolism destroys brain tissue.
7-73

Differential Diagnosis
Extracranial Causes: Pulmonary Disorders
Conditions That May Result in Hypoxia and Hypercapnia
Pulmonary hypertension
COPD Cystic & pulmonary fibrosis Pulmonary edema Pneumonia
7-74

Toxic inhalation
Cancerous tumors Tuberculosis Muscular dystrophy

Differential Diagnosis
Extracranial Causes: Cardiac Disorders

Numerous cardiac conditions are related to altered mental status:

Cardiac arrest Cardiac dysrhythmias Aortic stenosis Carotid sinus syncope Orthostatic hypertension Left ventricular failure Cardiogenic shock

7-75

Differential Diagnosis
Extracranial Causes: Diabetes Mellitus
Insulin-Dependent Diabetes (IDDM)
(complete absence of insulin secretion by pancreas)

Hypoglycemia
- Insulin administration without intake of glucose. - Blood glucose level usually less than 40 mg/dl.

Diabetic ketoacidosis (DKA)

- Lack of insulin results in accumulation of glucose in blood (hyperglycemia). - Ultimately leads to profound dehydration & acidosis.
7-76

Differential Diagnosis
Hypoglycemia vs. Diabetic Ketoacidosis
Hypoglycemia
Rapid utilization of glucose (OR lack of dietary glucose, post-insulin)

Relative surplus of insulin moves available glucose out of blood & into cells Drop in blood glucose produces immediate impairment of brain function
Sx: mentation, HR; pale, cool, moist skin, blood sugar <40 mg/dl.
7-77

Differential Diagnosis
Hypoglycemia vs. Diabetic Ketoacidosis
Diabetic Ketoacidosis (DKA)
Surplus of circulating glucose in undiagnosed diabetic (OR insulin-dependent diabetic who fails to take insulin) Relative glucose surplus draws water from cells, dehydrating tissues & gradually impairing all functions Sx: mentation, HR, BP, dry mucous membranes, poor skin turgor, Kussmauls respirations & fruity breath odor. Urine highly concentrated, ketotic

7-78

Differential Diagnosis
Extracranial Causes: Diabetes (continued)
Non-Insulin-Dependent Diabetes (NIDDM)
(inadequate insulin, or resistance to insulin utilization)

Hyperglycemic Hyperosmolar Nonketotic Coma (HHNC)

- Glucose rapidly exceeds ability of available insulin. - Partial nourishment occurs along with increase in blood glucose. - Similar to DKA, but acidosis does not occur. - Dehydration, electrolyte imbalance are main causes of altered mental status. - Blood glucose level often > 800 mg/dl.
7-79

Important to Note...
Hyperglycemic hyperosmolar nonketotic coma presents like diabetic ketoacidosis/hyperglycemia, except that ketone odors and Kussmauls respirations are not observed.

7-80

Assessment of Diabetic-Induced Altered Mental Status

Thorough Scene Size-Up
Note presence of items such as:
- Insulin containers - Other medications related to diabetes - Hypodermic syringes - Glucometers - Lower extremity prosthetic devices (Why?)

7-81

Diabetic Assessment
(continued)

Initial Assessment
Formulate general impression of mental status.
- Patient may not be aware of own diabetes. - Chief complaint may be confusion, restlessness, or weakness. - Confusion may prevent communication of diabetes. - If patient unresponsive, question bystanders.

Assess mental status. Evaluate and assure airway patency.

- Unresponsive diabetics may vomit, lose control of tongue. - Evaluate respiratory pattern (e.g., Kussmauls respirations).
7-82

Diabetic Assessment
(continued)

Physical Exam
Head
- Pupils (normal or dilated in hypoglycemia) - Orbits (sunken eyes in significant dehydration) - Oral cavity (degree of hydration) - Ketone odor (seen with DKA)

Chest - auscultation of breath sounds.

Abdomen - insulin administration sites.
7-83

Diabetic Assessment
(continued)

Physical Exam
Extremities
- Insulin administration sites - Medical alert jewelry - Slow-healing lesions - Distal neuropathy (sensory loss in extremities) - Poor peripheral vision - Provisional amputations - Scarring of fingers (as a result of blood sampling) - Poor skin turgor (decreased relative to hydration)
7-84

Diabetic Assessment
(continued)

Vital Signs
Respirations Pulse
- Normal or shallow in hypoglycemia or HHNC - Kussmauls respirations in DKA - Usually weak & rapid in DKA or HHNC - Rapid & full in hypoglycemia - Can vary, depending upon hemodynamic status - Low in later stages of DKA and HHNC - Usually normal in hypoglycemia

Blood pressure

7-85

Diabetic Assessment
Focused History

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Typical findings might include:

Weakness or lethargy Confusion Hunger, thirst or polyuria Chest pain, SOB, or dizziness (cardiac involvement) Nausea, vomiting, diarrhea General malaise Abdominal pain (electrolyte shifts)
7-86

Diabetic Assessment
Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Note & relay patient allergies.

7-87

Diabetic Assessment
Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Look for insulin or oral antihyperglycemics Determine if patient has been compliant in taking meds

Obtain and document patients meds

7-88

Diabetic Assessment
Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Be especially curious about:

Diabetes (IDDM or NIDDM) Cardiac disease Renal disease Vascular disease Obesity General history of diabetes Endocrine problems

7-89

Diabetic Assessment
Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Especially important in insulin-dependent diabetics Ask about frequency & amounts of food patient has been eating

7-90

Diabetic Assessment
Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Typical findings might include:

Gradual onset (DKA-3 days; HHNC-12 days) Acute onset (hypoglycemia) Weight loss Polyuria Polyphagia & polydipsia Exertion (rapid use of glucose) Vomiting (loss of food substance) Infection (increased use of glucose)
7-91

Management of Diabetic Complications

Field treatment varies, depending on the kinds of complications noted: DKA/HHNC

Hypoglycemia
Readily correctable in the prehospital setting by administering supplemental dextrose IV, IM or orally.
7-92

Treatment is geared toward rehydration and support of decreased respiratory & cardiac function.

Will require insulin & electrolyte adjustment at hospital.

Diabetic Management
Hypoglycemia
General supportive measures
Isotonic crystalloid at TKO rate Obtain blood specimen Determine blood glucose level

Intravenous Access

Cardiac Monitor
Treat arrhythmias if necessary Follow AHA guidelines
7-93

Diabetic Management
Hypoglycemia (continued)
Conscious Oral Dextrose
Food or drink Instant glucose

Lethargic/Stuporous/Comatose

50% Dextrose (25 g) IV

If no IV access, 1 mg glucagon IM Instant glucose

Give if patient malnourished Administer 100 mg IV or IM

7-94

Thiamine (vitamin B1)

Diabetic Management
Diabetic Ketoacidosis/HHNC
General supportive measures
Fluid boluses if fluid-deficient Administer 20 ml/kg boluses Watch for fluid overload

Intravenous Access

Cardiac Monitor
Treat dysrhythmias if necessary Follow AHA guidelines
7-95

Differential Diagnosis
Extracranial Causes: Hepatic Encephalopathy
Results from chronic or acute liver disease.
Failure of liver to convert ammonia to urea causes ammonia to accumulate. Toxic levels of ammonia can produce altered mental status (irritability, confusion, lethargy or coma).

Must be considered in patients with history of alcoholism, cirrhosis, hepatitis. If allowed to progress, will cause cerebral edema, necrosis, herniation & death.
7-96

Assessment of Hepatic Encephalopathy

Altered mental status Signs of liver failure
Jaundice (yellowing of skin or other tissue) Ocular icterus (yellowing of sclerae) Edema/ascites (fluid accumulation in abdomen) Fector hepaticus (musty odor on breath) Spider angiomas (spider-shaped networks of distended
capillaries at surface of skin)
7-97

Differential Diagnosis
Extracranial Causes: Uremic Encephalopathy
Results from kidney failure Metabolic wastes accumulate to toxic levels. Uremia causes alterations in mental status.

Body suffers electrolyte imbalances and fluid shifts Acidosis occurs

Without intervention, death will occur
7-98

Assessment of Uremic Encephalopathy

Altered mental status secondary to acidosis, electrolyte imbalance, and toxins Other signs of uremia:
Nausea and/or vomiting Cramping Neuromuscular disorders Malaise Kussmauls respirations
7-99

Management of Hepatic or Uremic Encephalopathy

Emotional support Stabilization of immediate life-threats Patent airway and oxygen IV crystalloids
Administer according to hemodynamic status. Avoid fluid overload in kidney failure.

Treat dysrhythmias as necessary.

7-100

Differential Diagnosis
Extracranial Causes: Acidosis & Alkalosis
Potential of hydrogen (ions) expressed as pH. pH value quantifies acid/base status. Most cells tolerate only a narrow range in pH. Normal human pH ranges from 7.35 - 7.45. If pH deviates even slightly, cellular damage or dysfunction occurs quickly.

7-101

Differential Diagnosis
Extracranial Causes: Acid-Base Imbalance
Alkaline pH 7.50 pH 7.45
HCO3 IONS HCO3 IONS H+ IONS

pH 7.40
H+ IONS

pH 7.35 pH 7.30 Acidic

7-102

Types of Acidosis
Respiratory Acidosis
Cells produce CO2 faster than lungs can excrete it. Retention of CO2 (hypercapnia) raises arterial CO2 level > 45 mmHg. pH drops accordingly, < 7.35.

Metabolic Acidosis
Metabolic acid production increases, or circulating bicarbonate levels decrease. HCO3 below 22 mEq/L drops pH to < 7.35.

7-103

Types of Alkalosis
Respiratory Alkalosis
CO2 is excreted faster than it is produced, and falls below a PaCO2 of 35 mmHg. Extracellular pH rises above 7.45.

Metabolic Alkalosis
Loss of hydrogen ions, or excess circulating bicarbonate levels. H+ ion concentration falls below normal, and increases extracellular pH to above 7.45.

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Common Causes of Acid-Base Disturbances

Disturbance
Respiratory Acidosis Metabolic Acidosis

Causes
COPD Asthma Narcotics OD Diarrhea DKA Anxiety Pulm. Embolus Vomiting Alkali ingestion Hypoventilation CNS Depression

Lactic acidosis Renal failure

Pregnancy Hyperventilation Gastric fluid loss

Respiratory Alkalosis Metabolic Alkalosis

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Assessment of Acid-Base Disturbances

Acidosis versus Alkalosis

Acidosis
Decreased LOC Lethargy, weakness, general malaise, confusion Pulse normal/slightly elevated early; slow & weak later Chest pain, anxiety or panic Hx of diarrhea

Alkalosis
Hyperexcited presentation Muscular spasticity, ataxia, inappropriate behavior Elevated pulses Chest pain, anxiety or panic Numbness or tingling in extremities Hx of vomiting
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Management of Acid-Base Disturbances

Definitive treatment of acidosis or alkalosis involves correction of the underlying cause -- usually in the hospital. Prehospital treatment usually includes
temporary stabilization of arterial pH, aggressive ventilation in respiratory acidosis, and management of other complications.
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Differential Diagnosis: Extracranial Causes

Electrolyte Imbalance: Sodium
Hypernatremia
Sodium plasma levels increase to > 145 mEq/L. Increased osmolarity results in cellular dehydration and shrinking.

Hyponatremia
Sodium plasma levels decrease to < 135 mEq/L. Osmolarity of extracellular fluid increases, shifts into intracellular space and causes cellular edema.
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Differential Diagnosis: Extracranial Causes

Electrolyte Imbalances: Calcium
Hypercalcemia
Serum calcium rises > 10.5 mg/dl. Excessive calcium results in decreased electrical impulse conduction, CNS depression.

Hypocalcemia
Calcium levels fall to levels < 9 mg/dl. Increased excitability within CNS (e.g., agitation, irritability, and sometimes tetany). Cardiovascular changes may occur. 7-109

Calcium
ECG Changes Affected by Calcium Imbalance
R Normal ECG tracing P Q S T

R
Shortened QT Interval (hypercalcemia) P Q S T

R Lengthened QT Interval (hypocalcemia)

P Q S T
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Assessment of Electrolyte Imbalance

Focused History

SAMPLE History
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Chest pain, dyspnea, dizziness (calcium) Palpitations (calcium) Nausea, vomiting, diarrhea (all electrolytes) Headache (hyper- & hyponatremia) Declining or improving mental or neurologic status Syncope (calcium)
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Assessment of Electrolyte Imbalance

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Note & relay patient allergies.

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Assessment of Electrolyte Imbalance

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Especially note the following:

Diuretics Potassium supplements Digitalis Beta blockers Thiazide diuretics

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Assessment of Electrolyte Imbalance

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Past history of electrolyte imbalances Diabetic ketoacidosis Kidney failure Parathyroid hyperactivity (hypercalcemia)

7-114

Assessment of Electrolyte Imbalance

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Last ingestion & recent history of food intake is important in gauging electrolyte intake.

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Assessment of Electrolyte Imbalance

Focused History (continued)

SAMPLE Questions
S igns & symptoms A llergies M edications P ast medical history L ast oral intake E vents prior to illness

Gradual versus acute onset Time of initial onset Improvement or deterioration of mental status Complaints preceding incident (headache, confusion, dizziness, falls) Cardiac complaints (chest pain, dyspnea, palpitations, syncope, weakness)
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Management of Electrolyte Imbalance

Correction of electrolyte disorders is complicated, and varies depending on severity and underlying causes.
Prehospital treatment is a function of identification, stabilization of life threats, and conveyance of critical medical information to the hospital staff.
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Differential Diagnosis
Extracranial Causes: Thyroid Disorders
Hyperthyroidism
Hypermetabolic state induced by excess levels of secreted hormones.

Hypothyroidism
Results from thyroid hormone deficiency.

Myxedema Coma
Severe complication of hypothyroidism caused by cold temperature, trauma, infection, stress, or any medication that depresses the CNS.
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Assessment of Thyroid Disorders

Hyperthyroidism versus Hypothyroidism

Hyperthyroidism
Hyperactivity, anxiety & paranoia Tachypnea Tachycardia Warm, flushed skin Goiter Exophthalmos Elevated pulse, resp., & BP History of weight loss, fever, infection, emotional stress

Hypothyroidism
Confusion, ataxia, LOC Bradypnea Bradycardia Cool skin Facial edema, JVD Lung sounds associated w/APE Decreased pulse, resp. & BP Cold exposure, unusual wt. gain, infection, drowsiness/weakness
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Management of Thyroid Disorders

Mild presentations of thyroid disorders do not require extensive prehospital intervention. (Clinically significant ones DO.)

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Differential Diagnosis
Extracranial Causes: Thyroid Deficiency
Wernickes Encephalopathy
Disruption of brain activity due to thiamine deficiency.
Should be suspected in elderly, alcoholics, destitute, or hypoglycemic patients unresponsive to dextrose. May be reversed with administration of thiamine.

Korsakoffs Psychosis
Neuronal damage due to long-term thiamine deficiency.
Results in major disturbances in memory and cognitive ability, and is irreversible.
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Management of Thiamine Deficiency

Wernickes encephalopathy typically responds to administration of thiamine (and D50, as necessary).
Draw blood, determine glucose level Administer thiamine: 50 mg IV & 50 mg deep IM If glucose level is low, administer D50, IV push

Korsakoffs psychosis does not respond to thiamine or D50.

7-122

Differential Diagnosis
Extracranial Causes: Toxic Encephalopathies
Barbiturates
Function by depressing activity of the RAS.
Toxicity depresses LOC & impairs sensory perception.

Higher levels of toxicity depress respiratory, cardiac & vasomotor centers.

Decreased respiratory activity produces hypoxia, hypercapnia & death.
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Differential Diagnosis
Extracranial Causes: Toxic Encephalopathies
Tricyclic Antidepressants
Prescribed for clinical depression, chronic pain, insomnia, and migraine headaches. Works by blocking reabsorption of norepinephrine & serotonin (responsible for feeling good). Toxic levels exert anticholinergic effects (SVTs, hypoventilation, hallucinations, coma). Antidysrhythmic properties depress myocardial automaticity & conduction. Hypotension results in cerebral hypoxia.

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Differential Diagnosis
Extracranial Causes: Toxic Encephalopathies
Phenothiazines
Used to treat psychotic behaviors such as schizophrenia, delusions, hallucinations, paranoia & Tourettes disorder. Decrease psychotic behavior by blocking dopamine receptors & via anticholinergic properties. Toxic levels result in vasodilation, cerebral hypoperfusion, and myocardial depression & conduction disturbances.
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Conditions Produced by Phenothiazine Toxicity

Acute Dystonic Reactions
Occurs within 48-72 hours of ingestion. Results in bizarre motor activity. Facial grimacing and tics. Neck twisting to one side (torticollis). Upward gaze; sometimes ocular paralysis. Reversible with treatment.

Tardive Dyskinesia
Results from long-term use. Exact mechanism is unknown. Represented by continual lip smacking, grimacing, scowling, tongue protrusion, and eyelid spasms. An irreversible syndrome with no known effective treatment.
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Differential Diagnosis
Extracranial Causes: Toxic Encephalopathies
Opiates and Opioids
Naturally occurring or synthetic narcotics typically used for pain management. Depress cerebral function & produce bradycardia, hypoventilation and vasodilation. Produce a variety of presentations ranging from stupor to coma. Pinpoint pupils are a key finding. 7-127

Differential Diagnosis
Extracranial Causes: Toxic Encephalopathies
Salicylates
Toxicity progresses in stages & depends on the amount ingested.

Hyperventilation occurs initially, producing respiratory alkalosis.

Excessive ingestion increases lactic acid, which precipitates metabolic acidosis. Acidosis produces delirium, hallucinations, stupor, and convulsions.
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Differential Diagnosis
Extracranial Causes: Toxic Encephalopathies
Carbon Monoxide
Colorless, odorless gas resulting from incomplete combustion of carbons. Competes with oxygen for binding sites on hemoglobin molecules of red blood cells. Cerebral hypoxia leads to headache, visual & auditory disturbances, cognitive deficits, delirium, drowsiness and/or agitation. Higher levels of CO produce seizures, coma, psychotic behaviors & death.
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Drugs Used for Toxicologic Emergencies

Agent
Syrup of Ipecac Activated charcoal Magnesium sulfate

Action
Gastric emptying Adsorbant Cathartic

Dose
30-60 ml 1-2 g/kg 30 g

Route
PO PO PO

Antidote
Acetylcysteine Glucagon Atropine Naloxone Diphenhydramine Flumazenil

Action
Acetaminophen Beta blocker Cholinergic Opiates Dystonic reaction Benzodiazepine

Dose
140 mg/kg 3-10 mg 2 mg 1-2 mg 20-50 mg 0.2 mg/30 sec.

Route
PO IV IV IV IV, IM IV

Differential Diagnosis
Extracranial Causes: Environmental Factors
Heat Exhaustion
Complication of heat gain & increase in body temp. Signs & symptoms include profuse sweating, headache, dizziness, syncope, confusion & delirium.

Heat Stroke
Dire emergency via extreme elevation of core temp. Temperatures greater than 105o F damage brain. Signs & symptoms include hot, flushed, dry skin; altered mentation; elevated vitals initially; and eventually shock, coma & cardiac arrest. 7-131

Differential Diagnosis
Extracranial Causes: Environmental Factors
Hypothermia
Body temperatures below 94o F impair bodys ability to generate heat. Temperatures below 85o F results in total hypothalmic dysfunction & loss of temp maintenance. Mental status can range from drowsiness to stupor to coma. May present with cool to cold, dry skin, and exhibit depressed vital signs. Bradycardia may occur with ectopic beats.

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Hypothermia
Changes on the Electrocardiogram
A J wave (Osborne wave) following the QRS complex is sometimes seen in hypothermia.
J wave J wave

Also sometimes seen in cases of hypercalcemia.

7-133

Differential Diagnosis
Extracranial Causes: Categories of Shock

Hypovolemic (many causes; e.g., hemorrhage) Obstructive (e.g., pulmonary embolus, cardiac
tamponade, tension pneumothorax)

Distributive (e.g., neurogenic, anaphylactic,

septic)

Cardiogenic (pump failure)

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Differential Diagnosis: What the History Says

Altered Mental Status

Environmental Factors

Findings
Hot/warm/cold Poor sanitation/nutrition, alcoholism

Possible Etiology
Heat/cold-related emergency (heat exhaustion/stroke, hypothermia) Electrolyte imbalance, Wernickes syndrome, Korsakoffs psychosis

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Differential Diagnosis: What the History Says

Altered Mental Status

Measurable Abnormal Findings

Findings
Blood glucose <40 mg/dl Blood glucose >300 mg/dl Cardiac dysrhythmia

Possible Etiology
Diabetes/hypoglycemia Diabetes/hyperglycemia Cardiac disease, stroke, intracranial tumor, electrolyte imbalance

7-136

Differential Diagnosis: What the History Says

Altered Mental Status

Abnormalities of Affect/Behavior/Mental Status

Findings
Bizarre behavior

Possible Etiology
Seizure, stroke, cranial infection, intracranial tumor, diabetes/hypoglycemia, alkalosis, Wernickes syndrome, Korsakoffs psychosis Diabetic emergency, hepatic/uremic encephalopaghy, acidosis, hyperthyroidism

Lethargy, malaise, confusion, decreased LOC

Hyperexcitability/hyperactivity

Alkalosis, hyperthyroidism

7-137

Differential Diagnosis: What the History Says

Altered Mental Status

Miscellaneous Remarkable Findings

Findings
Dialysis Shunt

Possible Etiology
Renal failure/uremic encephalopathy

Scarred fingers, slow-healing wounds, distal prostheses

Peripheral edema

Diabetes
Hepatic/uremic encephalopathy, electrolyte imbalance, hypothyroidism

Polyuria, polyphagia, polydipsia

Visual disturbances

Undiagnosed diabetes
Stroke, cranial infection, intracranial tumor, electrolyte imbalance

7-138

Differential Diagnosis: What the History Says

Altered Mental Status

Abnormalities of Motor Function

Findings
Ataxia, distal motor dysfunction

Possible Etiology
Stroke, cranial infection, acidosis/alkalosis, electrolyte imbalance, hypothyroidism, Wernickes syndrome/Korsakoffs psychosis, toxic encephalopathy, hypothermia Stroke, intracranial tumor

Decorticate/decerebrate posturing

7-139

Differential Diagnosis: What the History Says

Altered Mental Status

Pain

Findings
Chest pain

Possible Etiology
Cardiac disease, diabetes, hypo-/hyperglycemia, acidosis/alkalosis, electrolyte imbalance, hypo/hyperthyroidism, toxicologic encephalopathy, hypo-/hyperthermia Cranial infection (meningitis, encephalitis)

Neck pain or rigidity

7-140

Differential Diagnosis: What the History Says

Altered Mental Status

Remarkable Findings in the Skin & Surface Membranes

Findings
Diaphoresis

Possible Etiology
Diabetes/hypoglycemia, heat emergency Cranial infection (meningitis, encephalitis), hyperthyroidism Liver disease, hepatic encephalopathy Diabetes/hyperglycemia

Fever
Jaundice Poor skin turgor, dehydration

7-141

Differential Diagnosis: What the History Says

Altered Mental Status

Remarkable Facial Findings

Findings
Facial droop, dysphagia, deviation of the tongue, unilateral paralysis or weakness

Possible Etiology
Stroke, cranial infection, intracranial tumor, hepatic/uremic encephalopathy, electrolyte imbalance

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Differential Diagnosis: What the History Says

Altered Mental Status

Pharmacologic Observations at the Scene

Findings
Drug paraphernalia, open medication containers Syringes (note type) Injection sites

Possible Etiology
Toxic ingestion/OD, metabolic acidosis or alkalosis Diabetic emergency, toxic overdose Diabetes, toxic reaction/OD

7-143

Differential Diagnosis: What the History Says

Altered Mental Status

Abnormalities Noted in Breathing

Findings

Possible Etiology

Abnormal Breathing Patterns Stroke, cranial infection, intracranial tumor, hepatic/uremic encephalopathy, electrolyte imbalance, toxicologic encephalopathy Kussmauls respirations Metabolic acidosis, diabetic ketoacidosis Hypoventilation Respiratory acidosis, metabolic alkalosis Hyperventilation Respiratory alkalosis, metabolic acidosis Abnormal Breath Odors Fruity/ketone Musty Diabetes/diabetic ketoacidosis Liver failure/hepatic encephalopathy
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Altered Mental Status Treatment Pathway

Scene Size-up Observe patient presentation & clues such as medications, glucometer, home oxygen Initial Assessment Assess chief complaint, AVPU level of consciousness, ABCs. Note pathologic respiratory pattern. Assure patent airway, support respirations, oxygenation, and circulation as needed. Focused History & Physical Exam General supportive measures; O2, IV with isotonic crystalloid, draw blood & analyze glucose level, ECG & treatment of dysrhythmias per AHA, pulse oximetry, intubation as necessary. Administer glucose if hypoglycemic. Judicious fluid therapy as dictated by patients hemodynamic status; avoid overload. Consult standing orders & medical direction concerning specific drugs and treatments. Transport. Assess for Specific Etiology Treat the specific etiology

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C A S E S T U D Y F O L L O W-U P
Situation
Early in your shift, you respond to the residence of a male patient with altered mental status. On arrival, you are greeted by anxious family members who inform you that the patient is in an upstairs bedroom.

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C A S E S T U D Y F O L L O W-U P
Situation
History & Findings
While evaluating the scene for hazards, you make your way to the bedroom and find the patient supine on the bed, making loud gurgling noises. As you pass a nightstand, you note cigarettefilled ashtrays and medicine containers labeled Lovastatin and Vasotec.
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C A S E S T U D Y F O L L O W-U P
Findings
Cheyne-Stokes respirations (pulse-ox reading of 78%). Vomitus suctioned from hypopharynx. Decorticate posturing in response to painful stimuli. Right pupil is fixed & dilated; patient incontinent of urine. Right-sided facial droop; tongue deviated to right. Pulmonary rhonchi secondary to aspiration of vomitus. Left arm & leg are flaccid; no motor function. Sinus bradycardia without ectopy. Vitals: P=56, BP=240/158, and PPV at 18 breaths per minute.
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C A S E S T U D Y F O L L O W-U P
Treatment
Immediate, aggressive suctioning of hypopharynx. High-flow O2 therapy followed by tracheal intubation. Hyperventilate @ 24 breaths per minute. Establish IV with 0.9% normal saline at TKO. Draw blood specimens and evaluate blood glucose level. Place in semi-Fowlers position for prompt transport.

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C A S E S T U D Y F O L L O W-U P
Additional History
Family members state patient was raking leaves when he suddenly complained of severe headache. After coming into the house, he began vomiting and acting funny, and his speech became slurred. After 911 was called, patient became unresponsive. He has a PMHx of hypertension, high cholesterol, and smoking. He is on only two medications (Lovastatin & Vasotec); NKA. Last oral intake was at breakfast, 2 hours earlier.
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C A S E S T U D Y F O L L O W-U P
Findings & Treatment
Response to Care
Even though hypertensive, treatment w/ beta blockers is not an alternative due to bradycardia.

Patient continues to be monitored and managed until care is transferred to emergency physician at hospital.
Patient diagnosed w/ massive intracerebral hemorrhage.

Hospital staff able to reduce BP; patient taken for surgical evaluation. Prognosis is poor.
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