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CRRT - Indications
Continuous flow of blood through the hemofilter to remove fluid and solute AKI; When PT is hemodynamically unstable
CRRT - Assessment - fluid overload
I's and O's; Daily weights
Hemodynamic monitoring
Edema
Rising BP
Adventitious lung sounds
CRRT - Assessment - fluid deficit
ECF depletion; Decreased intravascular volume; Hemodynamic instability; hypotension
CRRT - Assessment - hemodynamic stability
Continuous VS monitoring
Watch for HYPOTENSION — r/t — Increased ultrafiltration rate; Blood leaks; disconnection
CRRT - Interventions for above clinical changes
Continuous VS monitoring
Watch for HYPOTENSION r/t
Increased ultrafiltration rate
Blood leaks
disconnection
AKI - Expected assessment findings of fluid overload
Edema
Increased volume
Rising weight
Hemodynamic changes
AKI - Expected assessment findings of fluid deficit
- ECF depletion
Decreased intravascular volumn
Decreased u/o — Oliguria; anuria
AKI labs
Serum creatinine
Creatinine clearance
BUN
Serum electrolytes
sodium
potassium
chlorine
Urine electrolytes
Fractional excretion of sodium
AKI - Interventions (for fluid balance and abnormal electrolytes)
Obtain IV access
Manage fluid balance
Admin IV fluids based on etiology
Crystalloids
NS
Colloids
Albumin
IVFV
Fluid restriction
Fluid removal
Restricted fluid intake based on etiology
Monitor
Potassium
Sodium
Calcium
Hypocalcemia
Replacement
non calcium based meds
Phosphorus
Hypophosphoremia
Dietary phos binding meds
Non aluminum based
Acidosis
Fluid balance
Hemodynamic values
Daily weights
I’s and Os
Electrolyte imbalance
Hyperkalemia
Hypocalcemia
Hyponatermia
Hyperphosphatemia
Acid base imbalances
AKI - Prioritization of emergent interventions
Avoid nephrotoxic medications; Electrolytes balance — Potassium — Hyperkalemia; Ecg changes; Sodium — hypoNA; hyperNA
Hyperkalemia management
EKG changes; Interventions based on priority
Heparin induced thrombocytopenia (HIT) - signs/symptoms
Neuro
Confusion
Headache
Impaired speech patterns
Hemiparesis or hemiplegia
Vision disturbances
Dysarthia
Aphasia
Ataxia
Vertigo
Nystagmus
Sudden decrease in consciousness
CV Chest
Diaphoresis
Pallor
Alterations in BP
dysrhythmias
Pulmonary s/s
Dyspnea;
Pleuritic pain
Chest pain
Rales
Chest wall tenderness
Erythema
Palpable cord
Pain on passive dorsiflexion of food, spontaneous maintenance of relaxed foot in abnormal plantar (homans sign)
Heparin induced thrombocytopenia (HIT) - Lab values
Platelet count — Less than 100,000mm^3^; Sudden drop of 50% from pts baseline after initiation of heparin therapy
Heparin induced thrombocytopenia (HIT) - Treatment/management
Medical
Monitor plt count
Discontinue heparin
Test heparin for antibodies
Direct thrombin inhibitors — Argatroban
Nursing
Decrease heparin exposure
Flush; Vascular access devices
Surveil for complications
DVT
Pulmonary emboli
Acute limb ischemia
Educate pt and family
Comfort and emotional support
Educate pts and family
DIC (disseminated intravascular coagulation) - Etiology
proteins that control blood clotting become hyperactive throughout the body
Always secondary to underlying condition
Gram negative sepsis -- 20%; Neoplasms
Obstetric complications
Massive tissue injury
Other causes
DIC (disseminated intravascular coagulation) - signs/symptoms
r/t hemorrhage
Gum bleeding
Venipunctures
Old surgical sites
Epistaxis
Ecchymoses
Hemoptysi
Hematuria
Abdominal distension
Hemorrhage
Subarachnoid hemorrhage r/t thrombi
Peripheral cyanosis
Gangrene
Dysrhythmias
Chest pain
Acute MI
Pulmonary embolus
Resp failure
Oliguria
AKI
Diarrhea
Constipation
Bowel infarct
ALOC
Ischemic stroke
DIC (disseminated intravascular coagulation) - treatment/management
Nursing
Support vital functions
Bleeding precautions
Comfort
Surveil for complications
Medical
Prevention
Maintaining organ perfusion
Slowing consumption of coagulation factors
Platelet transfusions
Distinguish between HIT and DIC - Assessment findings including lab values
HIT — s/s — Neuro s/s — Confusion; Headache\ Impaired speech patterns; Hemiparesis or hemiplegia; Vision disturbances; Dysarthia; Aphasia; Ataxia; Vertigo; Nystagmus; Sudden decrease in consciousness; CV s/s — Chest; Diaphoresis; Pallor; Alterations in BP; dysrhythmias; Pulmonary s/s — Dyspnea; Pleuritic pain; Chest pain; Rales; Chest wall tenderness; Erythema; Palpable cord; Pain on passive dorsiflexion of food, spontaneous maintenance of relaxed foot in abnormal plantar (homans sign); Labs — Platelet count — Less than 100,000mm^3^; Sudden drop of 50% from pts baseline after initiation of heparin therapy; DIC
Distinguish between HIT and DIC - Treatment differences based on priority concerns
HIT
Medical
Monitor plt count
Discontinue heparin
Test heparin for antibodies
Direct thrombin inhibitors
Argatroban
Nursing
Decrease heparin exposure
Flush
Vascular access devices
Surveil for complications
DVT
Pulmonary emboli
Acute limb ischemia
Educate pt and family
Comfort and emotional support
Educate pts and family
DIC
Medical
Prevention
Maintaining organ perfusion
Slowing consumption of coagulation factors
Platelet transfusions
Nursing
Support vital functions
Bleeding precautions
Comfort
Surveil for complications
Sickle cell anemia - Signs and symptoms
Low grade fever
Bone
Joint pain
Sickle cell anemia - Pathophysiology
RBCs form an abnormal sickle or crescent shape; Unable to carry adequate oxygen to tissues; Trapped in vasculature
Sickle cell anemia - treatment/management
Medical
Bone marrow transplant
Pain management
Prevent infection
Transfusion therapy
Admin of hydroxyurea
Nursing
Support vital functions
Vital signs
Hemodynamic parameters
I&Os
Lab values
Mental status
Skin
Comfort and emotional support
Surveil for complications
Educate pt and family
Hip and Pelvic Traumas: Complications
Hemorrhage
Exsanguination
Gait disturbances
Erectile dysfunction
GI tract trauma
His dislocation
Thromboembolic phenomena
1Including fat emboli
Hypovolemic shock
Immobility
Infection
Hip and Pelvic Traumas: Management
ABCs — HIGHEST PRIORITY
Can cause hypovolemic shock
Fluid volume status
Body weights
CNS parameters
Notify
Delayed cap refill
Tachycardia
U/O less than .5mL/kg/hr
Alterations in LOC
Hip and Pelvic Traumas: Identification
History — Injury
MVA — Safety restraint; Driver or passenger; Sit in jury description & location
Fall — Impact; Distance; Type of landing surface;
Pain — Tenderness; Inability to void; Pain;
Underlying medical disorders — Polycysic kidney disease; Frequent UTIs; Osteoporosis; Rheumatoid arthritis;
Med history — Corticosteroids; Tetanus immunization
Physical — Airway; Breathing; Circulation; Disability —
Neuro; Exposure — Underlying disease; Ensure C spine is IMMOBILIZED
Inspect — Abrasions; Pain and tenderness; Ecchymosis; Contusions; Lacerations; Groin; Genetalia; Suprapubic area; Frog leg positioning; instability
Hip and Pelvic Traumas: Complications, Management, identification
https://nursing.unboundmedicine.com/nursingcentral/view/Diseases-and-Disorders/73680/all/Pelvic%20Fractures?refer=true
FAST Ultrasound - Bed US
Suprapubic view
Checks Retroperitoneal space/bladder
RUQ
Checks hepatorenal space (Morison space) and diaphragm
LUQ
Check splenorenal space
Pericardial
Checks for tamponade
Trauma Surgery - Preop considerations
Resuscitation
IV access
Isotonic fluids
Blood products
AMPLE history
Allergies
Medications
PMH/pregnancy
Last meal
events/environment of injury
Correct coagulopathy
Acidosis
Hypothermia control
Trauma Surgery - Pre-op, Intra-op, and Post-op considerations - Intraop considerations
Damage control
Control hemorrhage
Control contamination
Definitive repair
Ongoing blood product administration
Temperature management
Complications
Major vessel injury
Tissue perfusion
Trauma Surgery - Pre-op, Intra-op, and Post-op considerations - Post op considerations
Ongoing hemodynamic monitoring
Trending of vital signs
Watch for continued bleeding, coagulopathy
and the lethal triad persisting into recovery
Pain management
DVT/VTE prophylaxis
Early mobilization
Monitor for infection at the surgical site and systemically
sepsis risk is elevated in trauma patients due to wound contamination, invasive lines, and mechanical ventilation
Watch for missed injuries —
rauma patients are at risk of injuries not caught in the initial survey due to patient factors
altered mental status
distracting pain
clinician factors
Flail Chest - s/s
Segment is apparent on visual examination
When breathing, goes in opposite directions — Lungs expand → chest sinks IN; Exhale → chest pokes OUT
Rapid shallow respirations
Tachycardia
Pain
Poor air movement
Asymmetrical chest movement
Crepitus on palpation of chest
Flail Chest - Management
Ensuring adequate ventilation
Supplemental oxygen
Intubation and mechanical ventilation may be necessary
Flail Chest - Complications
Underlying pulmonary contusion is common
Respiratory failure from inadequate ventilation
Atelectasis and pneumonia
Flail Chest - Identification
Results from fracture of several consecutive ribs, in 2 or more separate places, causing an unstable segment (\"rack of ribs\")
Instability of the segment causes paradoxical movement
the flail segment moves in the opposite direction from the rest of the chest wall during breathing
Management of open fractures - General principles
irrigation and debridement of the wound
tetanus prophylaxis
Antibiotics
surgical stabilization/fixation
Management of open fractures
Open fractures carry a high infection risk because of environmental exposure at the fracture site
Neurovascular status distal to the fracture must be assessed and monitored closely
Penetrating traumas - Management
Primary survey (ABCDE) first
airway, breathing, circulation with hemorrhage control
CT is the diagnostic standard
Bedside FAST ultrasound for rapid free-fluid screening
Surgical exploration/repair as indicated by injury location and severity
Penetrating traumas - Complications
Major hemorrhage and hemodynamic instability
Organ-specific injury
liver, spleen, hollow viscus, cardiac, vascular depending on trajectory
Infection
major risk of cerebral abscess if the skull/brain is involved or peritonitis/sepsis if abdominal organs are penetrated
Missed injury along the trajectory of the penetrating object
Penetrating traumas - Identification
Entry and exit sites
Bullet holes counted should be even
Discoloration, seat belt signs
Decreased bowel sounds
Cullens
Eccymosis around umbilicus
Greys turner
Ecchymosis to flanks
Distended abdomen
Peritonitis
Rebound tenderness
Kehrs sign
Pain in tip of shoulder due to presence of blood or irritants in peritoneal cavity
Tension Pneumothorax - Management
Needle decompression
Lung re-expansion to restore oxygen and ventilation
Removing air and or fluid from pleural space ASAP
Restoring negative pressure in chest cavity ASAP
Tension Pneumothorax - Complications
Untreated, progressive air accumulation compresses the heart and great vessels → leading to obstructive shock and cardiac arrest
Respiratory failure from inability to ventilate the affected lung
Tension Pneumothorax - Identification
Distended neck veins
Reduced breath sounds
Deviated trachea to the unaffected side
Hemothorax - Management
Lung re-expansion to restore oxygen and ventilation
Removing air and or fluid from pleural space ASAP
Restoring negative pressure in chest cavity ASAP
Hemothorax - Complications
Hemorrhagic shock from ongoing/large-volume blood loss
Retained hemothorax can lead to empyema or fibrothorax if not adequately drained
Hemothorax - Identification
Dyspnea
Tachypnea
Asymmetrical chest
Tachycardia
Decreased or absent breath sounds on the injured site
Chest pain
Decreased O2 stat
Hypotension in LATER stages
Glasgow Coma Scale Scoring - My Extra Value Meal Costs 4.56 - Eyes
Eyes — 1-4
1. None 2. To pain 3. To voice 4. spontaneous
Glasgow Coma Scale Scoring - Verbal
1-5
1. None 2. No words, only sounds 3. Words but not sounds 4. Disorientated conversations 5. Normal conversation
Glasgow Coma Scale Scoring - Motor
1-6
1. None 2. Decerebrate 3. Decoricate posture 4. Withdraws to pain 5. Localized to pain 6. Normal
Glasgow Coma Scale Scoring - Score
Mild brain injury — 13-15
Moderate brain injujry — 9-13
Severe - less than 8 — Less than 8 we intubate;
Intracranial pressure - s/s
Altered LOC
changes in GCS
pupillary changes
posturing (decorticate/decerebrate)
other signs of neurologic deterioration as ICP rises
Intracranial pressure - Management
Ongoing assessment of vital signs and hemodynamics
Recognize and reduce ICP
Maintain adequate cerebral perfusion pressure (CPP)
Suctioning as needed (carefully, since it can transiently raise ICP)
Capnography monitoring
Maintain normothermia
Control of environmental stimuli
Intracranial pressure - Complications
Herniation — one of the major causes of death from secondary injury after TBI.
Diffuse Axonal Injury - Def
Posttraumatic coma that is not caused by a mass lesion
It takes 12-24 hours to develop and may persist longer
Clinical signs
Decreased LOC
Increased ICP
Posturing
Global cerebral edema
90& remain in vegetative state
Treatment
Support of vital functions
TBI - Potential complications
Skull fracture
open (dura torn) or closed (dura intact); vault or basilar fractures; assess for Battle sign and CSF leakage (rhinorrhea/otorrhea)
Concussion
minor diffuse injury with brief LOC disruption, amnesia, headache, dizziness, nausea, irritability, poor concentration, impaired memory, fatigue
Contusion ("bruising of the brain")
from acceleration/deceleration injury, coup-contrecoup pattern, diagnosed via CT
Epidural hematoma
bleeding between skull and dura, often from middle meningeal artery laceration; classic presentation is brief LOC followed by a lucid interval, then a dilated/fixed pupil; treated with surgery
Subdural hematoma
acute (severe blow, altered LOC, unequal pupils, surgical), subacute (develops 4 days–3 weeks post-injury), or chronic (21+ days post-injury; may need craniotomy, burr holes, or catheter drainage)
Intracerebral hemorrhage (ICH)
bleeding deep within brain tissue; traumatic causes include depressed skull fractures, penetrating injury, or acceleration-deceleration; managed surgically or nonsurgically
Penetrating injury
missile injuries (GSW, knife, nail gun) causing focal damage; major risk of infection and cerebral abscess
TBI - Prophylaxis
preventing hypotension
hypercapnia
elevated ICP
maintaining normothermia
limiting environmental stimuli that could spike ICP.
TBI - Secondary injuries
Tissue ischemia
Hypotension
Hypercapnia
Cerebral edema
Spinal Cord Injuries - s/s
Airway
Stabilization
Spinal shock
Neurogenic shock
Spinal Cord Injuries - Management
Medical
Preserve neurologic function
Surgical
Stabilization
Decompression
Laminectomy
Spinal fusion
Pedicle screw fixation
Verbal plates
Bone grafting
Nonsurgical
Cervical
Immobilization
Fracture realignment
Tongs
Halo traction brace
Thoracolumbar injury
Immobilization
Nursing
Optimize hemodynamic stability
Assess, monitor, and trend the GCS score
Poikilothemy
Maximize psychosocial adaptation
Organ systems and complications
Resp status and airway
Bowel program
Urinary catheterization
Pressure injuries
Contractures
PRIORITIES PLEASE FOCUS ON
Optimizing hemodynamic stability
Preventing life threatening complications while maximizing the function of all organ systems
Spinal Cord Injuries - Identification
Dermatome mapping to localize the neurological level
ASIA Impairment Scale (A = complete, B–D = varying degrees of incomplete, E = normal)
CT and MRI for diagnosis; cervical spine clearance follows EAST guidelines based on whether the patient is awake/alert/neurologically intact vs. has pain, altered mental status, or is obtunded
Spinal Cord Injuries - Neurogenic shock
Occurs after cervical or high thoracic SCI due to loss of sympathetic outflow below the injury level, leaving parasympathetic tone unopposed
Presentation
bradycardia
hypotension
hypothermia/poikilothermy (loss of ability to regulate temperature) distinguishes it from hypovolemic shock, which presents with tachycardia
Management
hemodynamic support (IV fluids, vasopressors if needed to maintain adequate spinal cord perfusion pressure)
atropine or pacing for symptomatic bradycardia
temperature regulation
Spinal Cord Injuries - Autonomic dysreflexia
A medical emergency seen in SCI patients with injury at T6 or above, occurring after the acute phase once spinal shock resolves
Triggered by a noxious stimulus below the level of injury (most commonly bladder distention, also fecal impaction, skin breakdown, or tight clothing)
Presentation: sudden severe hypertension, bradycardia, pounding headache, flushing/diaphoresis above the injury level, and pallor/goosebumps below it
Spinal Cord Injuries - s/s, management, complication, and identification (including neurogenic shock, autonomic dysreflexia)
Danger signs of neurological decline following head injury
Drop in GCS score — even a 1–2 point decline matters; watch each component (eye opening, verbal, motor) individually, not just the total
Pupillary changes — a new dilated and/or fixed pupil, especially unilateral, is a hallmark of an expanding mass lesion (e.g., epidural hematoma) causing herniation
New or worsening posturing — progression from decorticate (flexion) to decerebrate (extension) posturing indicates worsening brainstem involvement
Deterioration after a lucid interval — classic for epidural hematoma: brief loss of consciousness, followed by a period of apparent normalcy, then rapid decline
Signs of rising ICP — altered LOC, vomiting, headache worsening, changes in respiratory pattern
New focal neurologic deficits or asymmetry — new weakness, sensory changes, or asymmetric findings not present on initial exam
Battle sign or CSF leakage (rhinorrhea or otorrhea) — suggests a basilar skull fracture and warrants close monitoring for meningitis risk
Vital sign changes tied to secondary injury — hypotension or hypercapnia, both of which worsen cerebral ischemia and edema
Seizure activity — a new seizure after head injury can signal worsening injury or increased ICP
Complications of Peptic Ulcer Disease - Assessment
VS
Increased HR
Decreased BP
Thready pulse
Increased RR
oliguria
Mental status changes
Peripheral pulse palpation
Urine output
Hematemesis
Hematochezia
Melena
H&H levels
Risk factors
H pylori
NSAID use
Liver cirrhosis
Obvious bleeding
Bloody vomit
Fresh BRIGHT red blood, “coffee grounds”
Melena
Black, tarry stools
Blood digestion in GI tract
Black appearance – due to iron
Labs
CBC
BUN
Electrolytes
PT/PTT
Liver enzyme measurement
ABG
Cross matching 4 blood
Test vomit and stool for gross and occult blood
Complications of Peptic Ulcer Disease - Treatment
Patent airway
Supplemental oxygen
Maintain BP
2 large bore caths
IV fluid resuscitation
Crystalloids
Colloids
Blood and blood products
Insert NG tube
Evacuate blood
Perform gastric lavage
Patient and family education
Complications of Peptic Ulcer Disease - Management of GI bleed
Medical
Neutralization or suppression of gastric acids
Airway protection
Fluid resuscitation
Correction of comorbidities
Nursing
Risk for stress ulcers and GI hemorrhage
Gastric pH measurement
Assess for signs of GI bleeding
Administer volume replacement
Initiate gastric lavage
Surveil for complications
Gastric Perforation
Educate the PT and family
Complications of Peptic Ulcer Disease - Management of hypovolemic shock
Assess for shock
Tachycardia
Weak pulse
Cool clammy skin
Hypotension
Prolonged cap refill
apprehension
Fluid resuscitation
Blood products PRN
Assess for shock — Tachycardia; Weak pulse; Cool clammy skin; Hypotension; Prolonged cap refill; apprehension; Fluid resuscitation; Blood products PRN
Complications of Peptic Ulcer Disease - Upper
Upper GI Bleed
Complications of Cirrhosis -Assessment
S/S
Jaundice
Headache
Hyperventilation
Mental status changes
Palmar erythema
Spider nevi
Bruises
Edema
Asterixis
Grading of encephalopathy
Complications of Cirrhosis - Management
Medical
Antibiotics
Lactulose
Nursing
Protect from injury
Surveli for complications
Resp depression
Cardiac arrest
Hourly neuro assessment
Educate pt and family
Complications of Cirrhosis - Treatment
Treatment
Complications of alcohol-related acute pancreatitis - Assessment
S/S
Sudden abdominal pain
N/V
Fever
Diaphoresis
Weakness
Tachypnea
Hypotension
Tachycardia
Physical
Hypoactive bowel sounds
abdominal tenderness
Guarding
Distension
tympany
Complications of alcohol-related acute pancreatitis - Management
Medical
Pain
Fluids
IV crystalloids and colloids
Nutrition
Enteral feedings
Straight into GI
Systemic
ARDS
AKI
GI bleed
Local complications
Pancreatic necrosis
Pancreatic pseudocyst
Nursing
Comfort & emotional
Pain management
Surveil for complications
Intraabdominal hypertension
Pancreatic infection
PT education
Dietary guidelines
Pancreatic enzyme replacement therapy
Diabetes education
Alcohol cessation
Pharmacology
Antacids
Histamine blocking agents
Gastric mucosal agents
Gastric proton pump inhibitors
Vasopressin
somatostatin
Fluid resuscitation
IV crystalloids and colloids
LR
Labs to monitor
Elevated ammylase
Elevated lipase
Prioritization
Liver failure - labs to monitor
Prolonged PT times
Elevated bilirubin levels
Elevated Aspartate aminotransferase
Elevated Alkaline phosphatase
Elevated Ammonia
Decreased serum albumin
Diabetic Ketoacidosis - Assessment
Clinical s/s
Malaise
Headache
Polyuria
Polydipsia
Polyphagia
N/V
Extreme fatigue
Weight loss
CNS depression
Dehydration s/s
Diabetic Ketoacidosis - Management
Monitor therapy response
Hourly BG
Hourly urine
I’s and O’s
VS
HR
BP
Hemodynamic values
Transition to SUBQ insulin
Surveil for complications
Hyponatremia
Cerebral edema
LOC
Skin care
Oral hygiene
Infection prevention
Diabetic Ketoacidosis - Treatment
SUBQ insulin
Fluids
Manage fluid balance
IV insulin
Treat underlying infections
Monitor acidosis
Monitor anion gap
Monitor and replace electrolytes
K, Mg, phosphate
Monitor serum bicarb
If low
Promote nutrition
Pt and family education
Diabetic Ketoacidosis - Labs to monitor
Hyperglycemia
Ketones
Acidosis
Diabetic Ketoacidosis - Prioritization
VS and labs
Blood glucose
Ketone blood and urine
Anion gap
Electrolytes
K, Mg
Blood pH
CO2/serum bicarb
Clinical assessment
Acetone breath (fruity)
Kussmaul breathing
Mental status changes
History and risk factors
New diabetes onset
On inulin or meds?
New infection onset
Acute illness onset
Assess for fluid balance deficits
Rule out pancreatitis
Hypothyroidism/Myxedema Coma - Assessment
s/s
Lethargic to coma
Low temperature
Brady cardia
Hypotension
Slow respiratory rate
Respiratory acidosis
Skin thickened, rough to touch
High TSH
Low free T4
Hypothyroidism/Myxedema Coma - Management
Medical
Ventilator support
Correction of F&E imbalance
Correction of multisystem abnormalities
Corticosteroid supplementation
Thyroid hormone replacement therapy
Nursing
Pulmonary
ABG monitoring
Dysrhythmias
ECG monitoring
Thermoregulation
Rewarming
Thyroid replacement therapy
Skin care
Elimination
Patient education
Hypothyroidism/Myxedema Coma - Treatment
Interventions
Intubation, mechanical ventilation depending on LOC, hypoxemia, hypercarbia, and metabolic derangement
Heat warmer to raise temperature
Normalize BP and HR
Administer hydrocortisone if associated adrenal dysfunction
Treat underlying infections
Correct metabolic abnormalities
Patient and family education
Hypothyroidism/Myxedema Coma - Pharmacology
Thyroid hormone replacement
Hypothyroidism/Myxedema Coma - Labs to monitor
TSH
Free T4
Metabolic pannel
Hypothyroidism/Myxedema Coma - Prioritization
Assessment
VS
BP
HR
Temp
History and RF
Hypothyroidism history
Thermoregulatory
Cold
Low temperatures
CV
Bradycardia
Hypotension
Neuro
Stupor
Coma
Seizures
GI
Constipation
GI ileus
Weight gain
Assess for associated endocrine dysfunction
Adrenal
pituitary
Diabetes Insipidus - Assessment
s/s
Dilute urine in high volume
Low urine osmolality
Low urine specific gravity
High serum sodium
High serum osmolality
Elevated ICP in central DI
ADH not produces
Diabetes Insipidus - Management
Medical
Volume restoration
Meds
DDAVP
Desmopresin
Nursing
Rapid fluids
VS
Urinary catheter
PT and family education
Diabetes Insipidus - Treatment
Priority interventions
Replace ADP
DDAVP
Vasopressin
Monitor U/O in response to vasopressin
IV fluid resuscitation
Crystalloids
Monitor serum sodium & osmolality
Monitor urine sodium & osmolality
Patient and family education
Diabetes Insipidus - Pharmacology
DDAVP
Vasopressin
Diabetes Insipidus - Labs to monitor
Serum osmolality
serum sodium
Urine osmolality
Urine specific gravity
Diabetes Insipidus - Prioritization
Assessments
VS
ICP
Urine output
Herniation
ICP elevation
Check pupils
Altered LOC
SIADH - Assessment
s/s
Dilution hyponatremia
Low serum sodium
Low serum osmolality
Low urine output
High urine sodium
Excess ADH produced
ADH level is not tested
SIADH - Management
Medical
Differentiate from other causes
Stop medication causing SIADH
Fluid restriction
500 to 100 mL/day
Sodium replacement
Osmotic demyelination
Medications
Vasopressin receptor antagonists
Vaptans
Aquadiuresis
Nursing
Fluid restriction
I&O
Labs
Moisten the mouth
Weight
SIADH - Treatment
Correct fluid and sodium balance
Restrict fluid intake
Pharm
Vaptans
Dont restrict fluids
Replaced sodium slowly
Do NOT raise more than 10mEq in 23 hrs
3%hypertonic sodium
0.9% crystalloid
Monitor serum sodium and osmolality
Monitor urine sodium & osmolality
PT and family education
SIADH - Labs to monitor
Serum sodium
Serum osmolality
Urine osmolality
SIADH - Prioritization
Assessments
VS
Mental status change
Seizures
Coma
High risk factors
Malignancies
Small cell carcinoma
Head injury
medications
SIADH - assessment, management, treatment, pharmacology, labs to monitor, prioritization
Pharmacology
HHS (hyperglycemic hyperosmolar state) - Assessment
s/s
Type II diabetes
Very high blood glucosis
Diuresis
Electrolyte imbalance
Normal acid base balance
Elevated serum osmolality
Dehydration
HHS (hyperglycemic hyperosmolar state) - Treatment
Priority interventions
Obtain IV access
Manage fluid balance
IV fluids based on level of dehydration
Insulin per protocol
Treat underlying infections
Monitor and replace electrolytes
K, Mg, phosphate
Monitor serum osmolality in HHS
Promote nutrition
Patient and family education
HHS (hyperglycemic hyperosmolar state) - Labs to monitor
Resolution
Serum osmolality <315
Anion gap normal
BG normal
Glucose
Ketone
pH
Osmolality
Sodium
K
Bicarb
Phosphate
Urine acetone