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DIABETIC KETOACIDOSIS (DKA)
Monitor for signs of increased ICP
Blood glucose level falls LOW or FAST before brain can equilibrate
Water moves from blood to CSF and brain
Cerebral edema and increase ICP
Hyperglycemic Hyperosmotic Syndrome (HHS)
a serious metabolic complication of diabetes mellitus ▪
formerly known as HHNK
Hyperglycemic Hyperosmotic Syndrome (HHS) Causes:
omission or sudden decrease in oral hypoglycemic dose
TPN or tube feedings without sufficient water
Renal disorder treatment (Peritoneal dialysis)
Hyperglycemic Hyperosmotic Syndrome (HHS) Clinical Manifestations:
similar with DKA but without the ketoacidosis
Hyperglycemic Hyperosmotic Syndrome (HHS) Treatment:
rapid fluid replacement to correct dehydration
Decrease glucose levels
DKA Onset, Triggers Manifestations
Onset
sudden
Triggers
infection
other stressors
inadequate insulin dose
Manifestations
Ketosis
Kussmaul’s respirations
“fruity” breath
nausea
abdominal pain
dehydration
electrolyte loss
polyuria, polydipsia
weight loss
dry skin
sunken eyes
soft eyeballs
lethargy
coma
HHS Onset, Triggers Manifestations
Onset
gradual
Triggers
infection
other stressors
poor fluid intake
Manifestations
Neuro symptoms
dehydration
electrolyte loss
DKA Laboratory
Serum Glucose
> 300 mg/dL
Osmolarity
variable
Serum Ketones
(+)
Serum pH
< 7.35
Serum HCO3
< 15 mEq/L
Serum Na
Low, N or high
Serum K
N, inc with acidosis
Low due to dehydration
BUN
> 20 mg/dL
inc due to dehydration
Creatinine
> 1.5 mg/dL
Urine Ketones
(+)
HHS Laboratory
Serum Glucose
> 800 mg/dL
Osmolarity
350 mOsm/L
Serum Ketones
(-)
Serum pH
> 7.4
Serum HCO3
< 20 mEq/L
Serum Na
N or low
BUN
increase
Creatinine
increase
Urine Ketones
negative
DKA Summary
Hyperglycemia
Metabolic Acidosis
Ketotic
HHS Summary
Hyperglycemia
Absence of Significant Acidosis
High Serum Osmolality
Hypoglycemia Nursing Intervention
Instruct to always carry some form of FAC
If no FAC is available, any food should be eaten;
high-fat foods ????
slow the absorption of glucose and the hypoglycemic symptoms may not resolve quickly.
Monitor for signs of HYPOGLYCEMIA UNAWARENESS
clients who may not experience warning signs of hypoglycemia until level is dangerously low
frequent episodes of hypoglycemia
older clients
taking β-adrenergic blocking agents
MYXEDEMA COMA
A rare but serious disorder results from persistently low thyroid production
Medical emergency with high mortality rate
Coma can be precipitated by:
acute illness
rapid withdrawal of thyroid medication
anesthesia and surgery
Hypothermia
Use of sedatives and opioid analgesics.
MYXEDEMA COMA Assessment
Hypotension
Bradycardia
Hypothermia
Hyponatremia
Hypoglycemia
Generalized edema
Respiratory failure
Coma
MYXEDEMA COMA Nursing Interventions:
Maintain a patent airway.
Institute aspiration precautions.
Administer as prescribed;
IV fluids (normal or hypertonic saline)
levothyroxine sodium IV
glucose IV
corticosteroids
Assess the client’s temperature hourly.
Monitor BP frequently.
Keep the client warm.
Monitor for changes in mental status.
Monitor electrolyte and glucose levels.
THYROID STORM
acute and life-threatening condition
in a client with uncontrollable hyperthyroidism.
Risk factors:
thyroid gland surgery and the release of thyroid hormone into the blood stream
severe infection and stress.
THYROID STORM Assessment:
Elevated temperature (fever)
Tachycardia
Systolic hypertension
Nausea, vomiting, and diarrhea
Agitation, tremors, anxiety
Irritability, agitation, restlessness, confusion,
and seizures as the condition progresses
Delirium and coma
THYROID STORM Nursing Interventions:
Maintain a patent airway and adequate ventilation.
Administer as prescribed;
Antithyroid medications : PTU
Iodides
Propranolol
Glucocorticoids : HYDROCORTISONE
Monitor vital signs. • Monitor continually for cardiac dysrhythmias.
Administer non-salicylate antipyretics as prescribed (salicylates increase free thyroid hormone levels).
Use a cooling blanket to decrease temperature
THYROID STORM Easy Nursing Interventions:
ABCs
Propranolol
1 mg IV
Propylthiouracil
1000 mg PO
Hydrocortisone
300 mg IV
Look for underlying cause
THYROID STORM Prevention:
Administration before thyroid surgery;
Antithyroid drugs
Beta blockers
Glucocorticoids
Iodides
Normal Intra Cranial Pressure
7-15 mmHg
The pressure exerted by fluids inside the skull, including cerebrospinal fluid and blood, on the brain tissue
Increased ICP
Increased Systolic BP
Decrease Pulse
Decrease Respirations
Shock
Decrease Systolic BP
Increased Pulse
Increased Respirations
Spinal Cord Injury (SCI)
Trauma to the spinal cord
Causes;
partial
complete disruption of the nerve tracts and neurons
Involves;
Contusion
Laceration
compression of the cord
Spinal Cord Injury (SCI) - Causes:
motor vehicle crashes
Falls
sporting and industrial accidents
gunshot or stab wounds
Spinal Cord Injury (SCI) - Result:
Spinal cord edema
compromised capillary circulation and venous return
SC necrosis
Spinal Cord Injury (SCI) - Sequela:
Loss of;
motor function
Sensation reflex activity
bowel and bladder control
Spinal Cord Injury (SCI) - Complications:
respiratory failure
autonomic dysreflexia
spinal shock
further cord damage
death
Most frequently involved vertebrae SCI
C5, C6 and C7
T 12
L1
REMEMBER IN SCI
Always suspect SCI when trauma occurs until this injury is ruled out.
Immobilize the client on a spinal backboard with the head in a neutral position
to prevent an incomplete injury from becoming complete.
SCI - Emergency Interventions:
Emergency management is critical
improper movement can cause further damage and loss of neurological function
Assess the respiratory pattern and maintain a patent airway
Prevent head flexion, rotation, or extension
During immobilization
maintain traction and alignment on the head by placing hands on both sides of the head by the ears
Maintain an extended position
Logroll the client
No part of the body should be twisted or turned, and the client is not allowed to assume a sitting position
In the ER, a cervical fracture should be placed immediately in skeletal traction via skull tongs or halo traction
to immobilize the cervical spine and reduce the fracture and dislocation
Spinal Shock
A complete but temporary loss of motor, sensory, reflex, and autonomic function that occurs immediately after injury
cord’s response to the injury
usually lasts less than 48 hours but can continue for several weeks
Peripheral neurons become temporarily unresponsive to brain stimuli
Neurogenic Shock
occurs most commonly in clients with injuries above T6
usually is experienced soon after the injury
Massive vasodilation occurs, leading to;
pooling of the blood in blood vessels
tissue hypoperfusion
impaired cellular metabolism.
Disruption of autonomic pathways → loss of sympathetic tone and vasodilation
Neurogenic Shock Assessment
Hypotension
Bradycardia
Spinal Shock Assessment
Flaccid paralysis
Loss of reflex activity below the level of the injury
Bradycardia
Hypotension
Paralytic ileus
Spinal and Neurogenic Shock Interventions:
Monitor for;
signs of shock following a spinal cord injury
hypotension and bradycardia
reflex activity
Bowel and urinary retention
Return of reflexes
Assess bowel sounds
Provide supportive measures as prescribed, based on the presence of symptoms
Autonomic Dysreflexia
Also known as autonomic hyperreflexia
It generally occurs;
after the period of spinal shock is resolved
injuries above T6 and in cervical lesions
Triggers;
visceral distention
distended bladder or
impacted rectum
It is a neurological emergency
Sequela:
hypertensive stroke
Autonomic Dysreflexia Assessment
Sudden onset
severe throbbing headache
Severe hypertension and bradycardia
Flushing above the level of the injury
Pale extremities below the level of the injury
Nasal stuffiness
Nausea
Dilated pupils or blurred vision
Sweating
Piloerection (goose bumps)
Restlessness and a feeling of apprehension
Autonomic Dysreflexia Nursing Priority Actions:
Raise the HOB and ask that the health care provider (HCP) be notified
Loosen tight clothing on the client
Check for bladder distention or other noxious stimulus
Administer an antihypertensive medication
Document the occurrence, treatment, and response.