Endocrinology System Disorders
Hormones are on a Pendulum:
- Patients are often stressed in the hospital – they may have increased cortisol, GH, epinephrine, glucagon;
In turn, they may have decreased insulin and therefore, hyperglycemia
Diabetes Mellitus
Diagnosis Criteria:
§ FPG ≥126 mg/dL (Fasting is defined as no
caloric intake for at least 8 hours)
OR
§ 2-h PG ≥200 mg/dL during OGTT.
OR
§ A1C ≥6.5%
OR
§ In a patient with classic symptoms
of hyperglycemia or
hyperglycemic crisis, a random
plasma glucose ≥200 mg/dL
Type 1 Diabetes:
§ Autoimmune mechanism +
environmental trigger in
genetically susceptible individuals
§ T Cell-mediated destruction
of pancreatic beta cells
§ Beta cell function will be
reduced by 80-90% before
hyperglycemia and other
symptoms will occur
§ Genetic predisposition
§ Onset occurs at any age
Genetics
§ TCF7L - affects insulin secretion
and glucose production
§ ABCC8 - helps regulate insulin
§ CAPN10 - associated with type 2
diabetes risk in Mexican Americans
§ GLUT2 - helps move glucose into the pancreas
§ GCGR - glucagon hormone involved in glucose
Type 2 Diabetes Pathophysiology:
- Beta cell dysfunction – impaired insulin secretion
- Alpha cell dysfunction – increased glucagon
- Increased hepatic glucose production
- Decreased incretin effect
- Increased lipolysis
- Increased glucose reabsorption
- Decreased glucose uptake in the muscle
- Neurotransmitter dysfunction
regulation
secretion
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Other types of Diabetes:
§ Pancreatic disorders (chronic pancreatitis)
§ Hormonal Disorders
§ Cushing disorder (excess corticosteroids)
§ Pheochromocytoma (excess catecholamines)
§ Acromegaly (excess growth hormone)
§ Other disorders
§ Cystic fibrosis - hyperviscous secretions, producing obstructive damage to many organs,
including the pancreas
§ Down syndrome
§ Hemochromatosis - autosomal recessive disorder characterized by increased iron absorption by
the GI tract and increased total body iron stores. The excess iron is sequestered in many
different tissues including the liver, the endocrine and exocrine pancreas, and the pituitary.
§ Drug Induced
§ Nicotinic Acid
§ Glucocorticoids- Steroids
§ Anti-rejection meds
§ HIV/AIDS meds
§ Chemotherapy
§ Infection/Trauma
Diabetes Management
- First line therapy: Metformin
o Mechanism of action
§ Reduce insulin resistance (liver > muscle)
§ Reduce hepatic glucose production
o Products available
§ Metformin, Glucophage XR, Glumetza
o Dosing:
§ 500 mg daily titration to 2000-2500 mg daily (start at low dose and work our way up)
o Side Effects: GI, Vitamin B12 deficiency
o Contraindicated: Metformin is contraindicated in patients with an eGFR <30 mL/minute/1.73
m2. (lactic acidosis with other nephrotoxic agents)
- Second line – assess complications to determine next step
o Generally, have some sort of cardiovascular complications. If so…
§ Put them on a GLP-I Receptor Agonist that does the following…
• Tells pancreas to make more insulin (increase biosynthesis) and not make
glucagon; increases B cell proliferation and decreases apoptosis)
• Works in brain to tell you that you are full (neuroprotective)
• Slows digestion – eat less
• Cardioprotective & increased cardiac function
• GLP-1Products available – “tide”
o Dulaglutide (Trulicity)
o Liraglutide (Victoza)
o Semaglutide (Ozempic or Rybelsus)
o Exenatide(Bydureon)
o Lixisenatide (Adlyxin)
• Dosing: Start slow and increase dose gradually
• Side Effects: GI
• Contraindicated: Some have renal adjustments
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§
§
§
§
Or… if HF or other cardiac issue, Put them on SGLT-2 inhibitor
• Prevents reabsorption of glucose in the kidney’s
• Cardioprotective as well for heart failure
• Products available – “flozins”
o Empagliflozin (Jardiance)
o Canagliflozin (Invokana)
o Dapagliflozin (Farxiga)
o Ertugliflozin (Steglatro)
• Dosing: Depends on goal of therapy
• Side Effects: GU infections (Fournier’s gangrene), dehydration, hypotension,
euglycemic DKA, NPO, bone fracture (canagliflozin)
• Contraindications: Renal dosing considerations
Or… if no cardiac issues, put them on Dipeptidyl Peptidase 4 inhibitor “liptins”
• Mechanism of Action: Slows the inactivation of incretin hormones by the DPP-4
enzyme
• Products available:
o Linagliptin (Tradjenta)
o Sitagliptin (Januvia)
o Alogliptin (Nesina)
o Saxagliptin (Onglyza)
• Dosing: variable, some are renally dosed
• Side Effects: severe joint pain; rash/blisters (bullous pemphigoid)
• Contraindications: NYHA class III or IV
Or if no cardiac issues, sulfonylureas “ides”
• Mechanism of Action: Stimulate functional beta cells
• Products available: Glyburide, Glipizide, Glipizide XL/ER, Glimepiride (Amaryl)
• Dosing: low and titrate as needed
• Side Effects: Hypoglycemia
• Other: Caution with renal or liver disease
Or if no cardiac issues, Thiazolidinediones “azones”
• Mechanism of Action: Decrease insulin resistance at peripheral sites and in the
liver
• Products available: Pioglitazone (Actos); Rosiglitazone (Avandia)
• Dosing: low and titrate up
• Side Effects: Edema, weight increase (10 lb)
• Other: + NASH, bone loss, bladder cancer
• Contraindications: NYHA class III or IV (don’t use in HF bc we are worried
about the edema SE)
Insulin Therapy
Basal Insulin
§ Intermediate or Long-acting insulin
§ Manages hepatic/renal glucose output
§ Never hold in the hospital bc provides general coverage
Bolus Insulin
§ Short or Rapid Acting insulin
§ Manages glucose excursions following meals or snacks
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§ Acute hyperglycemia or rise in BG post meal
Bolus Insulin Chart Options
Pre-Mixed Insulin Action
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Carbohydrate counting to determine insulin
The closer we can mimic normal glucose and insulin physiology, the more likely the glucose levels will be in
target range and avoid extremes of hypoglycemia and hyperglycemia. So, giving individually calculated
amounts of insulin for ingested carbs and for hyperglycemia more closely mimics the function of a healthy
pancreas.
Patient Education for Injection
§ Training pts on proper injections
§ Timing of injection
§ Rotation of sites
§ Upper outer thighs
§ Stomach
§ Buttocks
§ Upper, outer arms
§ Cloudy insulins needs to mixed
Diabetes Emergencies
Hyperglycemia
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Diabetic Ketoacidosis
Patho for DKA
- Absolute insulin deficiency OR stress, infection or insufficient insulin intake
o Increases glucagon, cortisol, catecholamines and growth hormone
o Increased lipolysis and glycogenolysis
§ Hyperglycemia
o Decreased glucose utilization
o Increased proteolysis
o Decreased protein synthesis
- Then we get FAA to the liver
§ Increased Ketogenesis – moderate serum ketones (should be negative)
• Increased in free fatty acid
§ Decreased Alkali reserve – CO2 goes down
§ Ketoacidosis
§ Lactic acidosis – increased in lactate level and anion gap à hyper osmolarity
- Glucuseuria (osmotic diuresis)
o Increased urine glucose and ketones in urine
- Dehydration
- Loss of water and electrolytes
- Impaired renal function
o Increased creatinine
Lab
Tests
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•
•
•
•
•
•
Basic Metabolic Panel
Magnesium
CBC
Routine UA
Serum Ketones
ABGs (Acidotic)
Additional Tests
• CXR
• EKG (Telemetry Monitoring)
• Lipase
• Hepatic Function Panel
• Serum Lactate
• Troponin
• Blood cultures x 2
• Urine culture
Physical Findings Comparison
Treatment of DKA / HHS:
- Monitoring
o Vital Signs every 1 hour
o Intake and Output
o Cardiac or telemetry monitoring
- Treatment:
o Bolus Fluids: 2 - 4 Liters 0.9% NS IV infused over 1 hour
o Maintance Fluids: 0.9% NS or 0.45% NS 150 -250 ml per hour
o DKA: When blood glucose is less than or equal to 250 mg/dl, replace IV infusion with D5 0.45% NS
at 150-250 ml/hr
o HHS: When blood glucose is less than or equal to 300 mg/dl, replace IV infusion with D5 0.45% NS
at 150-250 ml/hr
- Medication:
o Insulin: Bolus 10 units Regular insulin IV x1 and start IV infusion
- Additional: Treat any underlying patho (i.e. infection)
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A note about Potassium Administration
How do we know then HHS or DKA has resolved?
§ DKA has resolved when:
§ Mental status has recovered AND
§ BG <250 mg/dL
§ AG <12
§ Serum bicarb >18 mEq/L
§ Venous pH >7.30
§ In HHS, continue IVF and insulin IV gtt until pt’s mental status has recovered
HHS Pathophysiology
§ Hyperglycemia: BG > 600 mg/dL
§ Hyperosmolar: ↑ BG = an osmotic diuresis that leads to intravascular volume depletion, which is
exacerbated by inadequate fluid replacement
§ Non-ketotic: Still producing insulin
Physical Findings
• profound dehydration and hyperosmolality (effective serum osmolality > 320 – 330 mOsm/kg)
• hypotension
• tachycardia
• altered mental status
Causes
• serious, concurrent illness such as myocardial infarction or stroke
• sepsis
• pneumonia
• debilitating condition (prior stroke or dementia)
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Treatment of HHS is similar to DKA
§ Bolus Fluids: 2 – 4 Liters of 0.9% NS IV infused over 1 hour
§ Maintenance Fluids: 0.45% NS IV infused at 150 - 250 ml/hr
§ Medications:
§ Insulin Bolus: 10 units Regular Insulin IV x 1
§ Insulin Infusion
§ Treat any underlying patho
§ SubQ insulin if appropriate
Hypoglycemia
In general
§ Prolonged length of stay
§ Medical-legal implications
§ Centers for Medicare and Medicaid Services (CMS) “never events”
Pathophysiology – Release of Epi and Glucagon
• Glucagon
• Glycogenolysis→ gluconeogenesis → Increase hepatic glucose release
• Epinephrine
• Reducing glucose up-take
• Enhances production of hepatic glucose
• Occurs around 68 mg/dl
Neurogenic symptoms
§ Diaphoresis
§ Palpitations
§ Apprehension/ Anxiety
§ Tremor
§ Hypertension
Neuroglycopenic Symptoms
• Cognitive Impairment
• Fatigue
• Dizziness
• Visual Changes
• Seizures
• Hunger
• Inappropriate behavior
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•
•
Abnormal behavior
Convulsions
Risk Factors:
- Hypoglycemia unawareness
- Advanced age
- Chronic renal failure
- Liver disease
- AMS
Triggering Events
- Emesis / reduced oral intake
- Medication errors
- Severe illness
- New NPO status
- Severe illness
- Exercise
- Sudden reduction of steroid dose
- ETOH / drug use
Diseases of the Posterior Pituitary
§ Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
§ Excess ADH
§ Diabetes Insipidus (DI)
§ Deficiency of ADH
Syndrome of Inappropriate Anti-Diuretic Hormone:
Pathophysiology
- SIADH is an excess of ADH resulting in a physiologic imbalance of water.
- Here is what happens…
o Increased ADH àincreased water reabsorption in renal tubles à increased intravascular fluid
volume à dilutional hyponatremia and decreased serum osmolality
Etiology
§ CNS disturbances —stroke, hemorrhage, infection, trauma, and psychosis
§ Malignancies — Ectopic production of ADH by a tumor in small cell carcinoma of the lung; head and neck
cancer, olfactory neuroblastoma
§ Drugs — carbamazepine (Tegretol), high-dose cyclophosphamide (Procytox), and selective serotonin
reuptake inhibitors
§ Surgery —Transsphenoidal pituitary surgery; head injury
SIADH Clinical Manifestations
- Serum Sodium < 125 mEq/L:
o thirst, DOE, fatigue, HA, muscle cramps
- Serum Sodium < 120 mEq/L:
o GI: vomiting, abdominal cramps
o MS: Muscle twitching
o Neuro: cerebral edema, confusion, seizures, coma
- Physical Exam:
o No edema
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o Dry mucous membranes
o Decreased skin turgor
Diagnostic Criteria
SIADH Medical Management
§ Treat the underlying disease
§ Fluid restriction —intake of less than 800 mL/day
§ Except SAH
§ Correct Na+ Deficit
§ 3% NaCl – hypertonic solution
§ NaCl tabs – 2-3 grams TID
§ Loop diuretic or a vasopressin receptor antagonist
§ Demeclocycline—acts on the collecting tubule cell to diminish its responsiveness to ADH, thereby
increasing water excretion
Nursing Considerations for SIADH
§ Carefully monitor I/O
§ Daily weights
§ Fall precautions
§ Lower head of bed (Flat or <10 degrees)
Diabetes Insipidus:
DI Pathophysiology
§ Diabetes insipidus is a deficiency of ADH resulting in a physiologic imbalance of water either by:
§ neurogenic - insufficient production of ADH
§ nephrogenic - unresponsiveness of the renal tubules to ADH
§ Here is what happens…
§ Decreased ADH à Decreased reabsorption in renal tubules à Decreased intravascular volume à
excessive urine output and increased serum osmolality
DI Diagnosis
§ Goal – show that polyuria is caused by the inability to concentrate urine
§ Water deprivation test
§ Patient drinks fluids overnight and then deprived of fluids for 8 hours
§ Hourly monitoring of plasma osmolality and q2 hr urine osmolality
§ After 8 hours, pt is given desmopressin (DDAVP)
§ Confirmed to have DI if serum Osm > 305 mmol/kg
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Medical Management of DI
Neurogenic DI:
• Desmopressin (DDAVP) 20-40 mcg intranasally
qd – tid
Nephrogenic DI:
• Removal of underlying cause (ex. Lithium
therapy)
• Amiloride 5 mg/day for Lithium-related
disease
• Low sodium diet and chlorothiazide to
induce mild Na depletion
Nursing Considerations for DI
§ Carefully monitor I/O
§ Daily weights
§ Hypotonic IV solution
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ETOH Withdrawal Syndrome in Critically Ill Patients
1. What role do N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid (GABA) have with
alcohol withdrawal?
Ethanol affects a variety of neurotransmitter pathways and receptors in the central nervous system. Long-term
alcohol consumption creates an adaptive change to both the inhibitory γ-aminobutyric acid (GABA) and the
excitatory glutamate systems.6 Specifically, the downregulation of the GABA pathway results in reduced levels
of endogenous GABA, and reductions in the number and sensitivity of GABA receptors; activation of the
glutamate system occurs, too. N-methyl-d-aspartate (NMDA) receptors become upregulated, and the
concentration of the neurotransmitter glutamate increases. When alcohol consumption ceases, these processes
all lead to an unopposed neuronal excitation and the autonomic hyperactivity that occur during AWS.6
2. Look at table 2 in the article summarize how your patient could present based on last drink?
3. What is delirium tremens?
- The most severe and feared complication of AWS is delirium tremens, which is usually manifested within 2
to 5 days after the last drink.
- Patients with delirium tremens may have a fluctuating level of consciousness, with attention and cognitive
deficits, hallucinations, confusion, and hypertension.
- If delirium tremens is poorly managed, cardiovascular and respiratory collapse, arrhythmias, dehydration,
electrolyte imbalances, and multiorgan dysfunction may occur.
- The mortality rate for patients with untreated delirium tremens is high
4. What is the first thing a nurse would do with someone in alcohol withdrawal?
- Clean history
- Lab tests
- Assess current status
- Benzos first line therapy
5. What is the first and common medication used to treat alcohol withdrawal? How is it administered?
What special considerations would the nurse want to be aware of?
IV Benzodiazepines – assess for respiratory depression and additional nervous system depressants
6. What other medications could someone receive in alcohol withdrawal?
- dexmedetomidine
- phenobarbital
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-
antipsychotics
Propofol
Ketamine
IV fluids
treat nutritional deficits
7. What are inappropriate medications to give someone in alcohol withdrawal?
We believe they should not be used routinely in the treatment of moderate or severe alcohol withdrawal. Such
drugs include:
●Ethanol
●Antipsychotics (eg, haloperidol)
●Anticonvulsants (eg, carbamazepine)
●Centrally acting alpha-2 agonists (eg, clonidine, dexmedetomidine)
●Beta blockers (eg, propranolol)
●Baclofen
8. What other interventions would you include with your plan of care?
-
Resuscitation and rehydration
Vitamin and electrolyte replacement
Seizure precautions
Assessment and monitoring
Oncology
- Cancers can be classified into blood cancers or solid tumor cancers.
o Solid tumor cancers are differentiated by type with breast, prostate, colon, lung being some of
the most common.
o Liquid tumors or blood cancers comprise Leukemias, Lymphomas, and Plasma Cell disorders
(that include Multiple Myeloma).
Cancer Treatment
- Hormone therapy
- Surgery
- Bone marrow transplant
- Immunotherapy
- Radiation therapy
- Targeted therapy
- Chemotherapy
Blood Cancer
Acute Leukemia
- In acute leukemia:
abnormal blood cells are
immature blood cells
(blasts)
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-
o Can't carry out their normal functions, and they multiply rapidly, so the disease worsens quickly.
Requires aggressive, timely treatment.
Diagnose acute leukemia: peripheral blood tests (that’s where we see the blasts), a bone marrow biopsy, and
sometimes a lumbar puncture and imaging.
Differences between AML and ALL:
– AML: Fatigue, DIC, bleeding
– ALL: hepatosplenomegaly
– Lymphoid Lineage (ALL, Lymphomas,
CLL): More likely to have B-Symptoms
– Unintentional Weight Loss
– Drenching Night Sweats
– Fever of Unknown Origin
– Painless Lymphadenopathy
Treatment of Acute Leukemia
– Chemotherapy
– INDUCTION
– Meant to induce
remission
– Response to induction
can predict
outcomes/response to future treatment
– CONSOLIDATION
– Goal to eradicate disease that is below the level of detection
– Can be done with chemotherapy or stem cell transplantation
– MAINTENANCE
– Lower doses of treatment for prolonged periods of time to improve chances of cure
*** During Induction and consolidation, it is CRITICAL that we monitor patients for s/s of anemia,
thrombocytopenia, and neutropenia
Chronic Leukemia
– No blasts!
– Many types - Some produce too many cells and some cause too few cells to be produced
– Slow progression
– Involves more-mature blood cells - These blood cells replicate or accumulate more slowly and can
function normally for a period of time
– Forms of chronic leukemia initially produce no early symptoms and can go unnoticed or
undiagnosed for years.
– Chronic Lymphocytic Leukemia (CLL): B-Symptoms, early satiety, increased risk of infection
– Watch out for Hyperkalemia – it’s a red herring!
– Treated with
– BTK-inhibitors like Ibrutinib or Acalabrutinib
– BCL-2 Inhibitors like Venetoclax
– Chronic Myelogenous Leukemia (CML): Weakness, fatigue, SOB, fevers, bone pain
– Treated with Tyrosine Kinase Inhibitors (TKI) like Ponatinib, Imatinib, Nilotinib
Lymphoma
- arises in the infection-fighting cells of the immune system called lymphocytes (a type of white blood cell
made in the bone marrow).
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-
-
-
-
o Lymphocytes circulate throughout the body via blood and the lymphatic system.
Lymph nodes, a key structure of the
lymphatic system, are found throughout the
body and filter lymph fluid to remove
foreign particles.
o When bacteria and other
invaders are found in the lymph
fluid, lymphocytes multiply
within the lymph nodes,
including B cells, T cells, and
natural killer (NK) cells.
Lymphomas develop when these
lymphocytes transform from healthy to
malignant cells, therefore lymphomas can
be partly classified as B cell lymphomas
(the majority), T cell lymphomas, or NK
cell lymphomas (rare).
Hodgkin lymphoma has several
characteristics that distinguish it from
NHL, including the presence of ReedSternberg cells.
o These are large, cancerous, B cell-derived cells with a distinct appearance, named for the
scientists who first identified them.
o Hodgkin lymphoma is considered one of the most treatment-responsive cancer types with a
majority of patients—even those with advanced disease—being cured with standard therapies.
Non-Hodgkin lymphoma - diverse group of diseases distinguished by the characteristics of the cancer cells
associated with each disease type.
o Most people with NHL have a B cell type (about 85%).
o The others have a T cell type or a natural killer (NK) cell type of lymphoma.
o While NHL represents a more aggressive cancer diagnosis, some patients with fast-growing
NHL can be completely cured.
o Treatments for slow-growing NHL are effective in stabilizing the disease for long periods of
time, even years and decades.
Clinical Manifestations
- Symptoms of B-Cell Lymphoma (the most common) are the B-Symptoms we discussed earlier: drenching
night sweats, early satiety leading to weight loss, painless lymphadenopathy, fever of unknown origin
Diagnosis:
– Lymph Node Biopsy
– Imaging: PET/CT
– Peripheral Labs
– Bone Marrow Biopsy
Treatment:
– Immunotherapy
– Chemotherapy
– Radiation
– Stem Cell Transplant
– CAR-T Cell Therapy
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Multiple Myeloma
- Multiple myeloma is a cancer that forms in a type of white blood cell called a plasma cell.
o Healthy plasma cells help you fight infections by making antibodies that recognize and attack
germs.
- In multiple myeloma, cancerous plasma cells accumulate in the bone marrow and crowd out healthy blood
cells.
- The plasma cells make an abnormal protein (antibody) known by several different names, including
monoclonal immunoglobulin, monoclonal protein (M-protein), M-spike, or paraprotein.
Diagnosis of Multiple Myeloma
– Peripheral Labs for Myeloma Markers:
– Serum Free Light Chains
– Imunoglobulins
– M Protein
– Bone Marrow Biopsy
– PET/CT Imaging
Treatment of Multiple Myeloma
– NOT CURABLE
– Goal: Longest, deepest remission possible – how?
– Therapies:
– Immunotherapy
– Radiation
– Chemotherapy
– Stem Cell Transplant
– CAR-T Therapy
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Stem Cell Transplant
- SCT is the process of administration of CD 34 (stem
cells) into the host after a preparative
chemotherapy regimen
- Eradicates disease via high dose chemotherapy and rescue
the patient via administering stem cells and/or initiating
graft versus disease effect.
- New, healthy, effective immune system and functional
bone marrow providing hematopoiesis.
- The sources of the stem cells can be from the self:
o Autologous
§ Patient’s own stem cells
§ Collected after mobilization with highdose Neupogen (pheresis or surgical
bone marrow harvest)
- Or a donor:
o Allogeneic
§ Donor stem cell source
§ Matched Related donor (brother or
sister)- sib allo
§ Matched Unrelated donor (MUD)mud allo
§ Cord (fetal umbilical cord)- dual cord
§ Syngeneic (identical twin)
§ Haplo-identical (1/2 matched
donor)
Treatment Options for Stem Cell
- Autologous
o Lymphoma
o Multiple Myeloma
o CLL
o Amyloidosis
o Some autoimmune disorders
o Testicular
o Neuroblastoma
- Allogeneic
o ALL / AML / MDS
o Some refractory Lymphomas
o PNH
o CML/CLL
o Sickle cell disease
o Some autoimmune disorders
o Myelofibrosis
o Aplastic Anemia
Major Complications of Stem Cell Transplant
– Sinusoidal Obstructive Syndrome
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–
Graft Versus Host Disease - occurs when the donor’s T cells (the graft) view the patient’s healthy cells (the
host) as foreign, and attack and damage them.
– Chronic or Acute
– Chronic is a syndrome that may involve a single or several organs.
– One of the leading causes of medical problems and death after an allogeneic stem cell
transplantation.
– Can be fatal
– Affects: Skin, Gut, Liver, or anything else
– Prevention/Treatment: Steroids and Immunosuppression
CAR-T (Chimeric Antigen Receptor) Therapy
- Autologous chimeric antigen receptor (CAR) T cell therapy is a type of immunotherapy that genetically
modifies a patient’s own T cells to recognize and bind to specific proteins (tumor-associated antigens) on
the surface of antigen-expressing cells.
o manufactured for each individual patient using their own T cells.
- After a one treatment, CAR T cells can continue to multiply in a patient’s body (cell expansion) and have
the potential to remain in the blood for up to 1 year
- Evidence suggests that CAR T cell therapies stimulate a T cell response against antigen-expressing cells,
including normal and malignant cells.
o The external targeting domain binds to the antigen, activating the CAR T cell.
- Once activated, CAR T cells release cytokines and other soluble mediators that may play a role in the killing
of antigen-expressing target cells.
- Currently used in:
o Multiple Myeloma
o Lymphoma
o ALL (Acute Lymphocytic Leukemia)
CAR-T Therapy Toxicity - CRS
- Cytokine release syndrome (CRS)can occur in response to the over-activation of the immune systemin
response to Immune Effector Cell (IEC) engagement (such as CAR T-cells), with a supraphysiological
release of inflammatory cytokines, of which IL-6 plays a central role.
- Symptoms can mimic sepsis and be progressive including fever, hypotension, hypoxia and end organ
dysfunction.
- These can occur rapidly and without warning within the first 8 weeks (average at 5-7 days) after CAR T-cell
infusion.
- In severe forms, CRS can lead to potentially life-threatening complications such as cardiac dysfunction,
ARDS from capillary leak, renal or hepatic failure, DIC, or MAS/HLH (macrophage activation
syndrome/hemophagocytic lymphohistiocytosis).
- Run blood cultures, CBC, CRP and Ferritin
- FOR ALL neutropenic patients, hang antibiotics within one hour while you wait for cultures
- If Grade III or higher, Tociluzumab medication will be given; if symptoms don’t start to resolve or they get
worse, we will add steroids + Anakinra (IL 1 inhibitor)
- CRS + ICANS (below) can cause HLH and ARDS
ICANS (immune effector cell-associated neurotoxicity)
- More diverse adverse event associated with immune effector cells (IEC) and may involve blood-brain
barrier disruption, elevated levels of excitatory neurotransmitters as well as pro-inflammatory cytokines and
activated lymphocytes in the CNS.
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-
-
Symptoms of ICANS include aphasia, altered mental status, impaired cognition, motor weakness, seizures
or cerebral edema (Expressive aphasia appears to be a very specific symptom of ICANs, and
encephalopathy is a dominant feature)
o Non-specific symptoms such as headache, tremor, myoclonus, asterixis, hallucinations,
weakness, and intracranial hemorrhage have been excluded from grading.
The disorder can be mild, wax and wane, or become progressive.
Onset may be more delayed (i.e. 60 days out)
Recognition and early intervention of this adverse event can slow or prevent progression and improve
outcomes.
How to assess: name three objects, follow a command, ask them what year it is or who the president is
(time), who they are, where we are, count backwards from 100 + write a sentence (most accurate)
Oncologic Emergencies
– Any acute, potentially life-threatening event in the oncology patient
– Directly or indirectly related to cancer or treatment
– May develop at any stage of treatment
o Diagnosis
o Relapse
o Progression
– Delay in treatment may result in adverse outcomes
o Pain and suffering
o Death
– Immediate intervention is required
Categories
– Metabolic - TLS, Hypercalcemia, SIADH, Hyper/hypoglycemia
– Structural- SVC obstruction, Airway obstruction, Cord compression, Effusion, ñICP, Seizure
– Hematologic - Fever, Leukostasis/Viscosity, Bleeding, Thrombosis, DIC, CRS/ICANS
– Infusional - Extravasation, Anaphylaxis, Reactions
Metabolic Emergency – Tumor Lysis Syndrome
– Life threatening condition occurring after cellular destruction of rapidly growing tumors
– Release of intracellular components of tumor cells causing hyperkalemia, hyperuricemia,
hyperphosphatemia, secondary hypocalcemia, renal failure
– Typically, during first several days of chemotherapy but can occur spontaneously prior to chemotherapy
– Clinical TLS may result in rapidly progressing renal failure, seizure and cardiac dysrhythmia leading to
death
– Clinical Manifestation
– Most common in high grade, high bulk lymphomas, acute leukemias but can occur in low to
intermediate grade heme malig such as myeloma, CLL, etc.. Solid Tumor patients with high bulk
disease
– Hyperkalemia-release of intracellular potassium from tumor and can also be exacerbated by AKI
– Hyperuricemia-released from tumor, exacerbated by AKI and contributes to AKI crystal
obstructive nephropathy
– Hyperphosphatemia-Tumor cells contain up to 4X the inorganic phos than normal cells and this
is released with cell death, again exacerbated by AKI, and contributes to AKI when Calcium and
phosphate combine forming Ca/phos crystals and an obstructive nephropathy
– Hypocalcemia-secondary to increased phosphate binding, exacerbated by AKI and contributes to
direct tubular injury.
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Metabolic Abnormality
Clinical Manifestations
HYPERKALEMIA
Muscle cramps
Paresthesias
ECG changes
Bradycardia
Dysrhythmias
Cardiac arrest
HYPERPHOSPHATEMIA
Nausea/Vomiting/Diarrhea
Lethargy
Seizure
AKI
HYPOCALCEMIA
Muscle cramps
Tetany
Hypotension
Dysrhythmia
AKI
Chvostek’s and Trousseau’s sign to diagnose clinical hypocalcemia
(Trousseau’s is much more sensitive and specific)
HYPERURICEMIA
AKI
Monitoring these patients
- Need to monitor these patients very closely typically every 6-12hrs.
- some patients will be placed on the dialysis machine prior to chemo
- early notification of renal team is important
- beware of rasburicase in G6-PD, pregnancy, costly
- beware of 6-MP and azathioprine with allopurinol
- Alkalinization promotes the short-term excretion of uric acid but does not increase the solubility of xanthine
and hypoxanthine (products of cell nucleic acid catabolism which produce uric acid) thus could allow for
xanthine obstructive nephropathy.
o Alkalinization is controversial because it may cause metabolic alkalosis and calcium phosphate
precipitation
Clinical or Lab Abnormality
Intervention
HYPERKALEMIA
-avoid potassium supplementation
-NS infusion
-cardiac monitoring
Stabilize heart
-calcium gluconate
Shift potassium
-sodium bicarbonate
-insulin/D50
-albuterol
Remove potassium
-sodium polystyrene resin (kayexalate)
-dialysis
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HYPERURICEMIA
-allopurinol
-rasburicase
-NS infusion
-dialysis
HYPERPHOSPHATEMIA
-avoid phos and calcium supplementation
-NS infusion
-phosphate binder (sevelamer; aluminum hydroxide, calcium
acetate)
-dialysis
HYPOCALCEMIA
-if asymptomatic, no intervention
-if symptomatic, calcium gluconate
Metabolic Emergencies - Hypercalcemia of Malignancy (HCM)
– HCM is a complex metabolic disorder occurring in approx. 25% of cancer patients at some point during
course of disease
– Normally, calcium homeostasis is maintained by intestinal absorption, bone resorption and renal excretion.
In certain cancers this homeostasis can get out of whack due to renal dysfunction or hormonal
dysregulation.
– Most common in (breast, lung, squamous, myeloma)
– Classified as
– Mild(10.5-11.9mg/dL)
– Moderate(12-13.9)
– Severe(>14)
Organ System
Early Signs
Late Signs
Neurologic
Drowsiness, lethargy, weakness,
depression, confusion, delirium,
decreased DTR’s
Seizure, stupor, coma
Renal
Polyuria, polydipsia, e-lyte
wasting, dehydration,
nephrolithiasis, renal
insufficiency
Renal failure
Gastrointestinal
Anorexia, N/V, constipation,
abdominal pain, ulcers,
pancreatitis
Ileus, obstruction
Cardiovascular
ECG changes (prolonged
PR/QRS, shortened QT/ST,
bradycardia, arrhythmia)
Complete heart block, cardiac
arrest
Musculoskeletal
Muscle weakness, fatigue,
reduced muscle tone, bone pain
Ataxia, pathologic fractures
McCurdy & Shanholtz, Crit Care
Med (2012); Oncologic
Emergencies (2013)
To note:
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-
½ of serum calcium is protein so depending on a pt’s nutritional status a serum calcium may or may not be
the most accurate – ionized calcium is the gold standard to follow.
More info: (albumin) bound, therefore when albumin is low, there is a reduction in protein bound calcium
and an increase in the “active” free calcium, thus Calcium is actually higher that reported when corrected for
low albumin.
Structural Emergencies - Superior Vena Cava Obstruction Syndrome
– Compression or invasion of the SVC by tumor, thrombosis or infection causing obstruction of blood flow to
the heart from the head, neck, arms and upper thorax
– Occurs in 3-4% of cancer patients
– 80% caused by cancer (Lung cancers, lymphoma, thyroid, head and neck cancer, other metastases)
– Right sided lung cancers due to proximity to the SVC
– Especially primary mediastinal and other high-grade B-cell lymphomas
– Subclavian catheters
Clinical Manifestations
- Early signs
o Edema of face, neck, arms, thorax - Airway obstruction
o Dilated veins (spider veins)
o Facial plethora - Red, ruddy appearance to face and cheeks
o Horner syndrome - due to pressure on the cervical sympathetic nerves
- Late signs
o Cyanosis
o Absent peripheral pulses
o CHF, êBP, syncope
o Chest pain/SOB/resp. distress
o Hoarseness, stridor
o Mental status changes, seizure, coma
Treatment
– CT
– Tissue Biopsy
– Radiation +/- Chemotherapy
– Steroids
– Surgery/Vascular stenting
– Thrombolysis/anticoagulation
– Frequent VS, Tele Monitoring
Structural Emergencies - Malignant Spinal Cord Compression
– Occurs when malignant disease or pathologic vertebral fracture compresses spinal cord or cauda equina
– Affects 5-14% of patients with cancer
– Second most common neurologic complication in cancer
– May cause devastating neurologic disability and death
– New pain is the most common presenting symptom - Pain may be localized, radicular or referred.
– Tumor can occur extradural, intradural or intramedullary, most commonly extradural metastatic disease
– Can occur anywhere along the spine, but most common in thoracic spine (due to large amount of bone and
active bone marrow to support mets), followed by LS and then cervical spine.
– Diseases affect the most adjacent spinal column. Head and neck-affect cervical spine; majority affect
thoracic but commonly breast and lung CA; lower spine affected by prostate, colon, bladder, uterine and
renal CA.
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Level of Spine
Pain Location/Character
Clinical Signs
Cervical
Occipital headache and neck
stiffness
Radicular pain in neck, shoulder,
arm
Diaphragm weakness/paralysis
Neurogenic shock (hypotension, bradycardia),
paresthesias/paralysis, electric tingling sensation,
hyperactive DTR’s, autonomic dysfunction,
Horner syndrome
Thoracic
Localized and/or radicular pain in
chest and back
Abd. muscle weakness, leg weakness/paralysis,
band-like paresthesias, inc. DTR’s, +Babinski,
autonomic dysfunction
Lumbosacral
Localized and/or radicular pain in
groin or sciatic distribution in
legs, pain with straight leg raise
Pelvic muscle and leg weakness,
numbness/paresthesias, dec. DTR’s,
bowel/bladder dysfunction, impotence
Cauda equina
Localized, radicular or referred
pain in back and legs(s)
Cauda equina syndrome, muscle weakness, foot
drop, paralysis, decreased DTR’s, bowel/bladder
dysfunction, impotence
Treatment
– Aim is to alleviate pain, prevent permanent disability
– ROS/Physical exam (pain, neurologic impairment)
– Diagnostic Imaging Evaluation (MRI entire spine)
– Neurosurgical and Rad Onc consultation
– Dexamethasone
– Radiation
– Surgery (laminectomy, vertebral resection, kypho/vertebroplasty)
– Chemotherapy
Structural Emergencies - Malignant Pleural Effusion
– Malignancy associated collection of fluid in the pleural space
– Life threatening emergency affecting respiratory function through restriction of lung expansion, decreased
lung volume and altered gas exchange
– 50% of cancer patients may develop MPE
– Most commonly in lung, breast, lymphoma
– Associated with advanced disease and poor outcomes
Clinical Manifestations of MPE - Depends on speed of development, volume of effusion and underlying
lung disease
Subjective
– Dyspnea
– Dry cough
– Pleuritic chest pain
– Orthopnea/PND
– Hemoptysis, tracheal deviation
– Anxiety/fear of suffocation
– Fever
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– Malaise
– Weight loss
Objective
– Tachypnea
– Dullness to percussion
– Decreased/absent lung sounds
– Tracheal deviation (away)
– Egophony, êtactile fremitus
– Bronchial breath sounds
– Friction rub
– êdiaphragmatic excursion
– Cyanosis, accessory muscle use
Diagnosis:
– CXR-lateral and decubitus
– CT-detect smaller effusions; differential diagnoses
– US-to clarify volume of fluid and guide thoracentesis
– Thoracentesis
Treatment
– Treat underlying cause of effusion
– Chemo, XRT, antibx, diuresis, steroids, NSAIDs
– Therapeutic thoracentesis
– Chest tube drainage
– Pleurodesis/talc
– Pleuroperitoneal shunt
– Pleurex catheter
– Pleurectomy and pleural abrasion
*Expect your patient to need management of a drain, or have a wound post procedure
Infusional Emergencies - Hypersensitivity Reaction
– Reaction of variable severity occurring in response to the administration of chemotherapy, biotherapy or
supportive care therapies in cancer treatment
– Grade 1: urticaria, pruritis, rash, mild upper resp. symptoms
– Grade 2: grade 1+ wheezing, N/V, SOB
– Grade 3: grade 1/2+ serious cardiopulmonary or neurologic compromise
– Can be allergic (immunogenic) or nonallergic (nonimmunogenic)
– Multiple pathways likely contribute to hypersensitivity reactions
– Clinical signs range from mild hypersensitivity requiring no intervention, to severe
anaphylactoid/anaphylactic reactions leading to death
– Hypersensitivity reactions, despite the cause, are treated similarly
Prevention
– Pre-medication
o H1/H2
o Acetaminophen
o Corticosteroids
Treatment
– Cutaneous/Mild reaction
o slow or stop infusion
25
–
o H1/H2 blockers; +/- corticosteroids
o Demerol/dilaudid for rigors
Anaphylactoid reactions
o STOP infusion
o Epinephrine
o Corticosteroids
o H1/H2 Blockers
o Resuscitation (O2, fluids, nebs, intubation, pressors, etc.)
Infusional Emergencies – Extravasation
- Grades:
o Day 1-erythema and pain
o Day 4-erythema, swelling
o Day 8-blistering, swelling, beginning to slough
o Day 12-induration, necrosis, nerve, tendon damage
- Infiltration of a vesicant agent into surrounding tissue with potential to cause tissue destruction, nerve and
tendon damage and functional impairment
- Vesicants classified as DNA binding (worse) or non-DNA binding
- Certain risk factors pre-dispose patients to extravasation and preventative strategies are effective
- Vesicant extravasation is an emergency requiring immediate intervention and specialty consultation
Acute Management
– Stop the infusion (including chemotherapy and any other fluids)
– Do NOT remove the catheter/needle (disconnect IV tubing, but leave IV catheter/needle)
– Aspirate fluid (attempt to aspirate any fluid from the subcutaneous tissue through the IV catheter/needle)
– Do NOT flush the IV line/catheter
– If indicated, Sodium thiosulfate is the only antidote
– Elevate and immobilize the affected extremity (for 24-48 hrs.)
– Monitor the site closely (outline the extravasation area)
– Consultation/evaluation by plastic surgery team
Hematologic Emergencies - Disseminated Intravascular Coagulation
– Develops secondary to an underlying pathologic condition
– Coagulation disorder characterized by widespread intravascular thrombosis à tissue ischemia and organ
dysfunction and depletion of coagulant factors and platelets contributing to hemorrhage
– Cause: sepsis, trauma, obstetric conditions and malignancy
– Most common serious thrombotic disorder occurring in cancer
– Early recognition and immediate intervention are key
– These coagulation abnormalities are the result of the destruction of leukemic blast cells that release
procoagulant substances from the leukemia cells causing systematic activation of coagulation.
– This can cause microvascular clots and, in pts whose platelets are already low due to the
pathophysiology of the disease as we already discussed, increased platelet consumption, which can
lead to bleeding.
– In acute leukemia, DIC is associated with 10-40% of patient presentations.
– DIC in an acute leukemic patient is and oncologic emergency, but, in short, we simply need to
transfuse products so that the patient can keep up with her consumption demands until we can treat
the underlying leukemia.
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Clinical Manifestations
– Thrombosis is most common in solid tumors - Clot may pre-date CA diagnosis by months
– Bleeding occurs more often in Heme Malignancy
– Oozing from multiple sites, ecchymosis, petechiae, uncontrolled hemorrhage
– Microvascular thrombosis with hypoperfusion, ischemia, necrosis, organ failure
– Mental status changes, irritability, confusion - from microthrombi or intracranial bleed
– Cardiopulm decompensation, shock, MODS, death
Management
– Treat underlying cause of DIC (cancer, infection, trauma)
– Monitor DIC panel every 6-12hrs (cbc, dimer, fib, INR, PTT)
– Heparin anticoagulation if thrombosis predominates or for VTE prophylaxis if not contraindicated
– Blood product replacement
If PLT <10-20 (<30 if Heme
Malig and <50 if active
bleeding)
If INR >2
If Fibrinogen <100
If HGB <8
1U PLT
2U FFP
2U FFP or CRYO
1-2U PRBC’s
Hematologic Emergencies - Immuno-compromised Fever
– 80% of patients with a heme malignancy will develop FEVER
– 10-40% of solid tumor oncology patients will develop FEVER
– FEVER is a sign of INFECTION
– FEVER is a sign of SEPSIS
– FEVER may be the ONLY sign of INFECTION and impending SEPSIS
– SEPSIS may progress to SHOCK and DEATH
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–
Mortality rate nearly 30% and >50% in cancer patients - Leading cause of non-relapse mortality in patients
with cancer
Most Common Causes
• Gram negative bacteria
o Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, etc.
o Account for 40-50% of septic shock
o Typically, more pathogenic
– Gram positive bacteria
o Streptococcus, Staphylococcus, Enterococcus
o Account for 5-10% of septic shock
o Typically, less pathogenic
– Yeast/Fungal organisms
o Candida, Aspergillus, Zygomycetes
o Yeast/fungal - small percentage of septic shock, however very severe
– Viral
*In 20% of septic shock, organism not identified
Treatment
– Timeliness of interventions makes a difference
o reduces morbidity
o reduces mortality
o reduces hospital LOS
o reduces ICU interventions
o reduces healthcare cost
– Vital signs
o Volume resuscitation
o Oxygen support
– Labs - CBCd, CMP, PT/INR, fibrinogen, lactate
– Cultures - Blood (line/peripheral), urine, sputum, wound/lesions, abscess, etc.
– ANTIBIOTICS - DO NOT DELAY antibiotics for labs, diagnostic testing or any cultures OTHER
THAN blood cultures
– Diagnostic testing - CXR, CT, US, Bronchoscopy, etc.
Trauma
Emergency Severity Index
- Most major emergency organizations support the use of a 5-level triage system called the Emergency
Severity Index or ESI.
- Triage designations are made using severity of illness or injury and resource utilization.
- Patients coming into the ED are assessed and given a score by the triage nurse.
- Levels:
o ESI 1: without immediate intervention will likely decompensate. The threat to life is obvious in
this case. This can be due to uncontrolled hemorrhage, airway compromise, Respiratory
arrest/distress, or a myriad of other reasons.
§ IF vital signs are outside of normal must consider upgrading to ESI 2
o ESI 2: are considered high risk.
§ Would you give your last open bed to this patient? Examples include suicidal ideation
patients, sexual assault victims, and physically aggressive patients.
§ High risk/ decreased LOC/Severe Pain or confused, lethargic, or disoriented
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•
Pain that is out of proportion to their injury / mental status that suddenly becomes
altered
o IF the patient does not fall into either of these categories then the clinician must ask how many
resources will be utilized.
o ESI 3 is the most common designation for those coming to the ED.
§ These patients require more than 2 resources.
o ESI 4 patients: one resource; ESI 5 patients - no resources
Emergency Assessment
- Assessment in the ER is different than the standardized head to toe
- Assessed for threats to life using a Primary Survey… then assessed using a focused assessment based on
chief complaint.
- Trauma patients are assessed in a more systematic manner using the primary secondary followed by a
secondary survey.
o This allows caregivers to address threats to life and find any concurrent injuries.
Primary Survey
• Goal is to identify and treat life threatening conditions
• Can be identified at any point during the survey - If at any point a life-threatening condition is identified
then interventions must be initiated regardless of where you are in the assessment process.
• ABC’s may need to reprioritize to
• The primary survey consists of Airway, Breathing, Circulation, Disability, Expose and
Environmental control, Full set of vital signs/family presence, and get resuscitative adjuncts.
• <C> refers to catastrophic hemorrhage
Airway/Alertness/C-Spine upon arrival
• AVPU – Alert, Verbal, Pain, Unresponsive
• If the patient responds normally, they are alert.
• If they respond only to voice, they are alert to verbal stimuli.
• If the patient requires painful stimuli to respond like a sternal rub, then they alert to pain.
• The patient is unresponsive if they do not respond to any of the above stimuli.
• Progress from least to most invasive airway management method
29
•
•
Open the Airway using a jaw thrust maneuver / remove any possible obstruction
• Patient who is unresponsive more likely to require ET intubation using a rapid sequence
technique. This uses sedation and paralytics to prevent possible aspiration and airway trauma.
Stabilize cervical spine during airway management - Always assume that a trauma patient with injuries
to head, neck, or upper torso has a cervical spine injury and maintain cervical spine stabilization
throughout assessment.
Breathing
• Assess Breathing (rate, depth, symmetry)
• An assortment of injuries can cause deficits to respiratory status including rib fractures, pneumothorax,
and penetrating injury.
• Interventions would include endotracheal intubation, chest tube placement, and needle thoracostomy.
• Administer supplemental oxygen - administer 100% O2 (non re-breather) to the trauma patient due to
increased metabolic demand.
• The trauma team must always be prepared to assist ventilations with 100% O2 if the patient’s
breathing decompensates at any time.
Circulation
• Check a central pulse to assess quality and rate
• Assess skin for temperature, color, moisture, & perfusion deficits including capillary refill.
• A prolonged capillary refill would also be a sign of shock.
• Administer blood products to replace lost blood volume
• When assessing circulation, the trauma team actively searches for signs of hemorrhagic shock
• Assessing a central pulse usually a carotid.
• A weak thread pulse would be a sign of shock and bleeding suspected
• Trauma patients often require massive transfusion for lost blood volume.
• Adequate IV access is imperative to deliver large volumes over a short amount of time.
• Two large bore IV catheters are inserted into the antecubital space or above bilaterally.
• Large bore is considered a 16-to-14-gauge catheter.
• Uncrossmatched blood is given - This
consists of type O negative blood.
Disability – AVPU (alert, verbal, pain, unresponsive)
• Assess LOC using the Glasgow Coma Scale
• If the GCS is 8 or less the likelihood that the
patient cannot control their own airway is
suspected. The saying goes “less than 8
intubate”
• Assess pupils
• Size, shape, equality, and reactivity
Exposure and Environmental Control
• Remove clothing
• Do not remove impaled objects
• Keep the patient warm - warm blankets, use warmed
blood and fluids when possible and raise the temperature
in the trauma room.
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Fully Set of Vitals and Family Prescence
- Obtaining a full set of vital signs will allow the trauma team to make informed decisions regarding the
treatment plan.
- Diagnostic procedures will most likely be delayed until patients are hemodynamically stable.
- Family presence during resuscitative efforts is encouraged according to recent research.
o Family members report that being present allows them to take a more active role in the care of
their loved one.
o It is important that a member of the trauma team be with the family at all times to answer
questions and explain procedures.
Get Resuscitation Adjuncts
• Measures are taken to monitor the patients condition on an ongoing basis.
• Use the pneumonic LMNOP
• L = Labs - blood typing, Hemoglobin and Hematocrit, and ABG’s
• M = Cardiac Monitoring
• N = Naso or Orogastric tube - nasogastric tubes are contraindicated when head or facial trauma is
known or suspected.
• O = Pulse Oximetry and end tidal CO2 monitoring
• P = Pain Assessment and Management
Secondary Survey
- The secondary survey is a brief systematic process to identify all injuries.
- The secondary survey only begins after all components of the primary survey have been addressed and
lifesaving interventions have been started.
History and Head-to-Toe
• Talk to EMS personnel
• Scene details can provide valuable insight to guide assessment - The mechanism of injury can focus
assessment efforts and interventions by predicting certain injuries based on details of the accident.
• SAMPLE
• S = Symptoms
• A = Allergies
• M = Medication History
• P = Past Health History
• L = Last Oral Intake
• E = Events leading to injury
• Head/Neck/Face – gaze, bruising, bleeding, JVD
• Chest – paradoxical movement, crepitus, breathe sounds
• Abdomen/Flanks – bruising, bowel sounds, distension, FAST exam (bedside US for peritoneal bleeding)
• Pelvis/Perineum – palpate for stability, bleeding, priapism, rectal tone
• Extremities – crepitus, deformity, pulses, compartment syndrome
Inspect Posterior Surfaces
- The final step in the trauma assessment is to inspect posterior surfaces.
- The trauma patient must be logrolled using at least 3 people. One person maintains inline cervical spine
stabilization while the remaining two trauma team members cross arms and roll the patient onto their side.
- The posterior surface is inspected for bruising, abrasions, wounds, or deformity.
Ongoing Monitoring and Evaluation
- All interventions must be reevaluated throughout the trauma assessment process.
31
-
Assessment must be repeated with any change to evaluate status
Interventions are reevaluated starting with airway, breathing, and circulation.
Level of consciousness is reassessed and appropriate action taken for any change in status.
Patients are transported for diagnostic tests to further evaluate or taken to the operating room for emergency
surgery.
o Surgery is definitive treatment for all life-threatening trauma.
o That means we must do all we can to get the patient to the OR! What I mean by that is that the
patient can die during the primary survey if we do not act quickly and methodically.
Targeted Temperature Management
• Indicated for post cardiac arrest patients who achieve ROSC - Cardiac arrest codes are a common
occurrence in any ER. Many are brought in by ambulance and have resuscitation efforts started in the field.
• Early defibrillation and good chest compressions are the aim of any cardiac arrest code.
• If ROSC or return of spontaneous circulation is achieved the patient is a candidate for targeted
temperature management.
• Cooling the patient’s core temperature to 32 to 34 degrees Celsius for 24 hours post resuscitation is
associated with a decreased mortality rate and improved neurological function.
• Target temperature is 32 to 34 degrees Celsius
• Associated with decreased mortality and improved neurological function
Death in the ED
• Common occurrence in critical care
• RN plays a significant role in providing comfort
• Organ and tissue donation
Geriatric Patients
• The aging population in the United States is growing and the elderly make up 43% of all ER visits.
• It is important to inquire if the patient has an advanced directive when they arrive to the ER.
o Many elderly patients have explicit instructions in the event they are incapacitated and cannot
make medical decisions.
• The elderly population is at increased risk for injuries and illness.
o One of the most common injuries are fractures related to falls. It is important to illicit the source
of the fall as this can often be the result of a medical condition like a stroke or heart attack.
32
Heat Related Injuries
• Heat related injuries occur when the thermoregulatory mechanisms in the body fail due to exposure to
ambient heat. As a result, the patient’s core temperature will begin to rise.
• Increased core temperature can lead to heat cramps in large muscle groups. This is usually associated
with strenuous sport or exercise and occur once the athlete rests. Rest for 12 hours usually resolves the
cramps along with sodium and electrolyte replacement via sports drinks.
• Heat Exhaustion can occur to prolonged heat exposure and is associated with escalating symptoms like
hypotension, nausea/vomiting, confusion, and profuse diaphoresis.
o Usually occurs due to prolonged strenuous outdoor activity.
o Treatment begins by removing the patient from the environment and removing constrictive
clothing.
o The patient may need intravenous normal saline to correct dehydration and hypotension.
• Heatstroke is the most serious heat-related emergency.
o This condition results from a failure of the thermoregulatory mechanisms in the hypothalamus.
o Rapid fluid and electrolyte loss due to diaphoresis cause sweat glands to stop functioning.
o As a result the body is unable to cool itself and core temperature increases rapidly.
§ A temperature above 105.8 degrees Fahrenheit is indicative of heatstroke.
§ The skin will be hot, red, and dry.
§ The patient will also exhibit a range of neurological symptoms including altered mental
status, loss of muscle coordination, and combativeness.
o The patient is at risk for a direct thermal injury to the brain as a result of cerebral edema and
hemorrhage.
o Treatment includes stabilizing ABC’s and reducing core temperature. Regardless of the cooling
method it is important to control patient shivering to prevent an increase in core temperature.
Cold Related Injuries
-
Cold-related injuries can be localized like frostbite or systemic in the case of hypothermia.
Frostbite is the formation of ice crystals in the tissue as a result of exposure to freezing ambient
temperatures.
o The body responds with peripheral vasoconstriction which decreases blood flow.
o As ice crystals form in interstitial tissue cell membranes are destroyed and cause edema.
33
-
o Superficial frostbite involves the skin and subcutaneous tissue such as fingers and toes. Skin can
appear blue or mottled and is crunchy and frozen to the touch.
§ Treatment for superficial frostbite is to immerse in a warm bath of circulating water.
Handle the tissue gently and never massage or scrub the affected area.
§ Re-warming can be painful and analgesia may be needed.
o Deep frostbite involves muscle, bone, and tendon.
§ Skin can be white and hard and skin mottling can turn into gangrene if not treated.
§ Treatment involves rewarming in a circulating warm water bath and then elevating the
extremity to reduce edema.
§ The extremity may be amputated if tissue damage is too severe.
Hypothermia is a core temperature below 95 degrees Fahrenheit.
o Both conditions are caused when the heat created by the body cannot overcome the heat lost by
the body.
o Mild hyperthermia presents with shivering, lethargy, and confusion.
o Moderate hypothermia causes body rigidity, slowed respirations, hypotension, and shivering
diminishes. The heart is especially irritable to the drop in core temperatures and is prone to
dysrhythmias.
o Severe hypothermia is a temperature below 89.6 degrees Fahrenheit.
§ Severe hypothermia makes the person appear dead.
§ Vitals are difficult to obtain.
§ The patient must be warmed to at least 86 degrees before death is pronounced.
§ The cause of death is usually recurrent ventricular fibrillation.
Drownings
• Defined as respiratory difficulty after submersion in water
• Most victims are less than 5 years old or males aged 15-25.
• If water is aspirated pulmonary edema develops - Laryngospasm often prevents victims from aspirating
water, but if fluid is aspirated pulmonary edema rapidly develops.
• Treatment focuses on correcting hypoxia with aggressive airway control.
• Assume there is a cervical spine injury present
Stings and Bites
• Severity is based on direct tissue damage or toxins
• Wasp, bee, and hornet stings can cause localized pain or life-threatening anaphylaxis.
• Ticks can transmit neurotoxins that cause Lyme disease
• Animal bites cause mechanical destruction to tissue that can lead to infection
• Treatment includes scraping the stinger away from the body with a fingernail or credit card and removing
any restrictive clothing.
• Ticks attach themselves to a host and inject a neurotoxin that causes disease. Lyme disease is the most
serious of these diseases and can lead to an ascending paralysis that causes respiratory arrest.
• The treatment is to remove the tick using forceps. Muscle function is restored within 42 to 72 hours
after tick removal.
• Animal bites cause mechanical destruction to tissue, blood vessels, and bone. These bites can lead to
infection or rabies transmission.
• Rabies prophylaxis treatment is indicated if the animal was unprovoked, or the animal is not found.
Poisoning
• Any chemical that harms the body is a poison
• ingested, inhaled, absorbed through the skin, injected, or splashed in the eye
• Severity is based on type of chemical and what route it was ingested
34
•
Goal of treatment is to decrease absorption, enhance elimination, and administer any toxin specific care
• Gastric lavage is one method of decreasing absorption by removing the substance from the
stomach.
• A large diameter tube is inserted into the stomach.
• The stomach is irrigated with copious amounts of sterile saline.
• The contents of the stomach are then drawn out using a large syringe.
• It is imperative that those with altered LOC or absent gag reflex are intubated prior to
gastric lavage to prevent aspiration of substances into the lungs.
• Gastric lavage should be performed less than one hour from ingestion.
• Activated Charcoal binds to ingested toxins and prevents absorption.
• Administered orally or via a gastric tube within 1 hour of ingestion of toxic substances.
• This is the most common and effective method to prevent absorption.
• Hemodialysis may be required if the toxic substance causes the patient to become acidotic.
Violence
- Every patient who enters the ED is screened for Family and Intimate partner violence (IPV).
o Common assessment questions are “do you feel safe at home?” and “Is anyone hurting you?”
- SANE nurses are specially trained and certified to collect and document evidence in sexual assault cases.
They provide emergency care and advocate for the victims.
- The ED is a high-risk area for healthcare worker assault by patients.
- It must be understood that the ED consists of the general public in a high stress dynamic environment.
o Some under the influence of drugs and alcohol / mental health disorders
Mass Causality Incident
• Is an emergency that overwhelms a community’s ability to respond with existing resources
• 30% of victims will require admission / 50% of those will require surgery
• Victims are treated, stabilized, decontaminated and transported
• Can be man-made (terrorism) or natural (hurricane)
• Large number of victims
• Multiple agencies respond
Triage for MCI
- Triaging victims is the responsibility of the first responders to the MCI.
o Differs from the ER triage we discussed earlier.
o Completed in 15 seconds for each patient.
- Colored tags are used to determine the order that patients will be treated and transported to a hospital.
o Green is given to patients who are ambulatory and have minor injuries.
§ This is the “walking wounded” category.
o Yellow - urgent but do not require the next ambulance that is leaving the scene.
o Red tags - immediate life-saving intervention and will require the next ambulance to leave the
scene.
o Black tags - not breathing or have sustained injuries that will cause them to expire before they
reach the hospital. Example (Massive head trauma)
- This system is designed to do the best for the most victims.
- The system works like this.
o All ambulatory patients are told to walk to a safe area away from the scene. These patients are
given a GREEN tag.
o Next assess patients for spontaneous breathing.
§ If the patient is not breathing open the airway using a jaw thrust maneuver.
§ If the patient starts breathing after airway repositioning the patient is a RED tag.
35
o If the patient does not start breathing, then they are a BLACK tag.
o If the patient is breathing, then respirations are estimated at either over 30 or under 30 per minute
(45 for pediatrics).
§ If respirations are over 30 than the patient is given a RED tag (assessing for shock)
§ If respirations are under 30 than the patient’s perfusion is assessed by taking their radial
pulse.
o If the radial pulse is absent, then capillary refill is assessed.
§ If capillary refill is over 2 seconds, then the rescuer controls any bleeding and gives the
patient a RED tag.
o If capillary refill is under 2 seconds or the patient has a radial pulse, then mental status is
assessed by determining if the patient can or cannot follow commands.
§ If the patient cannot follow commands, they are a RED tag.
§ If the patient can follow commands, they are a yellow tag.
o Mental status
§ Cannot follow simple commands – red tag
§ Can follow simple commands – yellow tag
Shock
What is shock?
• Decreased tissue perfusion and impaired cellular metabolism
• Lack of oxygen=↑ anaerobic cellular metabolism
• Results in an imbalance between the supply of and demand for oxygen and nutrients.
• It is a clinical syndrome not a disease
• Problem with pump, volume, or vessels
• The cause of shock can vary, but the physiologic response of the cells due to hypoperfusion are similar.
• Septic shock is the most common type of shock among patients admitted to the intensive care unit.
• Cardiac output is heart rate x SV and SV is altered by several factors like preload, contractility of the
heart and afterload.
• These three mechanisms within stroke volume can alter how much blood will be ejected out of
the heart.
Four types
1) Cardiogenic: pump failure – issues with the heart or pump
2) Hypovolemic: decrease intravascular volume
3) Distributive: misdistribution of circulating blood volume
a) Neurogenic shock: loss of sympathetic tone
b) Anaphylactic shock: massive hypersensitivity response
c) Septic shock: overwhelming inflammatory response
4) Obstructive: physical blockage of blood flow
Assessment of Cardiac Output
Pre-load – volume indicator
• Weight, I/Os
• UO
• VS
• Edema
Afterload
• Vasoconstriction, vasodilation
• BP
• Skin assessment – cold and clammy vs. red and sweating
• Peripheral pulses
36
Contractility
• Echocardiogram
CO is used to evaluate contractility, but it is
difficult to pinpoint actual cause of low CO
• Decreased contractility from direct
myocardial insult
• Inadequate myocardial stretch from
preload being too low
• Overstretched myocardium from
preload being too high
• Low afterload (vasodilation)
• High afterload (vasoconstriction)
Difficulty to measure volume in ventricles,
so we us pressure to estimate volume
• Pressure indicates stretch and volume
1) Preload: CVP, PAWP
2) Afterload: SVR/PVR
Organ Perfusion Measures
• Perfusion measured by BP and MAP
• RN orders to titrate
• MAP> 65mm HG or greater
(MAP >60mmHG needed to adequately perfuse and sustain vital organs)
• SBP >90 mm HG
• Minimal basis to support BP based on old research that kidneys don’t produce urine below
60 mm HG
• Pulse Pressure
• SBP-DBP
• Normal=40
• <40= vasoconstriction
• >40 vasodilation
Cardiogenic Shock
What is it?
• Pump failure
• Systolic or diastolic dysfunction→ decreased stroke volume→ reduced CO
• Causes
• MI (systolic dysfunction) – leading cause of death from acute MI
• Cardiac tamponade or cardiomyopathy (diastolic)
• Structural issue (valvular disorder)
• Dysrhythmia
• Clinical Manifestations
• Similar to decompensated heart failure
• Tachycardia, hypotension, narrow pulse pressure
• ↑SVR
• Increase in pulmonary wedge pressure
• Tachypnea
• Crackles
37
•
•
•
•
Signs of peripheral hypoperfusion
Cyanosis, pallor, diaphoresis, weak peripheral pulses, cold/clammy skin
↓urine output
Anxiety, confusion, agitation
Hypovolemic Shock
What is it?
• After a loss of intravascular fluid volume, inadequate circulating volume
• Fluid deficit
• Absolute hypovolemia=loss of fluid d/t hemorrhage, GI, DI, diuresis
• Relative hypovolemia= fluid out of vascular into extravascular (third spacing) d/t increased capillary
permeability like in burns
• Look at the progression of VS over continued loss of blood.
• Realize smaller and ill individuals may show class II signs and symptoms with just a 10% loss.
• Patho: ↓intravascular ↓venous return ↓decrease preload ↓SV ↓CO
• Body compensates for 15% of total body volume
• 15-30% results in SNS response
• ↑HR, CO, RR
• ↓SV, CVP, PAP
• Clinical manifestations
• Anxious, ↓ UO
• How do we treat it?
• General treatment for stage I/II: crystalloid fluid replacement and stage III/IV: crystalloids and/or
blood.
Hemorrhagic Shock
Classes
• Class I: (up to 15%) ≤ 750ml, S/S-normal BP/RR/UO, HR≥100, minimal to no change, anxious
• Class II: (15-30%) 750-1500ml, ↑SNS-mediated response: S/S-Increase CO, HR 100-120, ↓PP, RR: 2025, ↓CVP, PA pressure, U/O: 20-30ml/hr, restless
• Class III: (30-40%) 1500-2000ml, significant ↓BP, HR >120, RR: 25-30, U/O 5-15ml/hr
• Class IV: (≥40%) >2000ml, S/S-DECREASED BP (SBP <90), HR>120, ↓PP, RR 30-40, U/O: minimal
to no U/O, Confused, lethargy, loss of autoregulation in microcirculation and irreversible tissue
destruction.
Distributive Shock
• Misdistribution of blood flow and volume
• 3 subcategories
• Neurogenic Shock
• Anaphylactic Shock
• Septic Shock
Distributive – Neurogenic Shock
• Occurs within 30 minutes of spinal cord injury (can last for six weeks)
• Loss of SNS vasoconstrictor with massive vasodilation – tissue hypoperfusion
• Causes
• T6 or above**
• Epidural anesthesia
38
•
• Drugs (opioids/benzos)
Clinical Manifestations
• Hypotension
• Bradycardia
• Unable to regulate body temperature (warm dry skin from pooling of blood in extremities)
Distributive – Anaphylactic
• Hypersensitivity reaction to a sensitizing substance
• sudden
• Massive vasodilation → ↑capillary permeability→ edema→ bronchospasm
• Major increase in capillary permeability= relative hypovolemic state
• Causes
• Drug, chemical, vaccine, food, insect venom
• Contact, inhalation, ingestion, or injection
• Clinical Manifestations:
• Dizziness
• Chest pain
• INC
• Swelling of lips & tongue
• Wheezing
• Stridor
• Bronchospasm
• Flushing
• angioedema
Distributive – Septic Shock
• Systemic inflammatory to a suspected infection
• Hypotension despite adequate fluid resuscitation
• Septic shock is a subset of sepsis with profound circulatory, cellular and metabolic abnormalities
• Inadequate tissue perfusion
• Microorganism enters body→ normal immune response →immune response exaggerated →
↑inflammation & coagulation → microthrombi
• Causes
• Unknown organism 50%
• Gram-negative and gram-positive bacteria*
• Parasites, fungi, virus
• Clinical Manifestations d/t
• Vasodilation
• Misdistribution of blood flow
• Myocardial depression
• D/t
• May be euvolemic but d/t vasodilation become hypovolemic and hypotensive
• EF decreased first few days →ventricles dilate →maintain stroke volume
• Initially hyperventilates →respiratory alkalosis →uncompensated turns to respiratory
acidosis
Obstructive Shock
• Physical obstruction to blood flow with a decrease CO
• Causes
39
•
•
Impaired ventricular filling or emptying
• Cardiac tamponade, tension pneumothorax, abdominal compartment syndrome, stenotic
aortic valve, PE, right ventricular thrombi
Clinical manifestations
• Decreased CO, increased afterload, jugular distension, pulses paradoxes (see an abnormally large
drop in SBP, greater than 10mmHG, with inspiration)
Stages of Shock
1. Initial stage - During the initial stage symptoms are generally not clinically apparent but at a cellular
level the body is experiencing aerobic to anaerobic metabolism causing lactic acid buildup.
2. Compensatory
1. Body attempts to regulate with
neural, hormonal, biochemical,
compensatory
2. Multisystem response
1. ↓CO → ↓ BP and narrow
pulse pressure →activate SNS
→stimulates vasoconstriction
→ ↑HR, contractility, BP →
dilate coronary vessels
2. ↓ BP activate SNS →
angiotensin II → H2O and
NA reabsorption, K excretion
3. Ventilation perfusion
mismatch →increase RR
4. GI →impaired mobility
→paralytic ileus
5. Cold and clammy skin*
6. Cause of shock not correct
patient enters progressive
stage
3. If compensatory mechanisms are
supported patient can stay in this
stage for hours without sustaining
permanent damage
4. A Person can pass through this
stage so quickly so it is important
to recognize the symptoms of
shock, because it can spiral out of
control.
1. While all of this occurring
you might only see a bit of
raised HR, increase in
RR and some underlying
anxiety or change in
LOC.
3. Progressive (see graphic to the right
“Pulmonary & Cardiovascular” and below
“GI”)
1. As compensatory mechanisms fail
40
2. Life-threatening emergency
3. Massive SNS response
1. Profound vasoconstriction
4. Hallmark: ↓BP ↑RR, ↑HR, LOC listless, agitated
5. Frequently this is when patients receive interventions
6. Change in mental status is an important finding
7. During this time there is complete deterioration of the cardiovascular system: cardiac CO falls,
BP drops, and there is altered capillary permeability which can lead to anasarca (diffuse
profound edema).
4. Irreversible / Refractory
1. The arterioles-capillaries system or cellular mitochondria cease functioning as a result of acute
or persistent hypoxia
2. The refractory stage has decreased perfusion from peripheral vasoconstriction and decreased CO.
3. Lactic acid increases and fluid is leaving the vascular space causing hypotension and
tachycardia.
4. During this stage they have profound hypotension and hypoxemia.
5. Recovery is unlikely in this stage.
6. Failure of many organs leads to increase waste products
1. Lactate, urea, ammonia, carbon dioxide
A couple of important notes:
• Patients have difficulty tolerating compensatory changes associated with shock:
• HTN, Elders, kids, cardiovascular disease, DM with vascular issues
• There are still negative things happening in all organ systems even though compensated.
• The word compensated does not mean ideal or good. It means you are holding your own, but you can get
better or worse if the underlying problem does not get reversed
System
Compensatory Stage
Progressive Stage
Irreversible Stage
Neuro
A&Ox3, restless,
apprehensive,
Change in LOC, less
responsive, listless,
agitated
Unresponsive. Areflexia, pupils
nonreactive
CV
Narrow pulse pressure,
­HR, slight ¯BP but
adequate
­Cap permeability
¯BP, ­HR MAP <60
¯pulses
¯CO, hypotension, arrhythmias
Resp
­ RR, resp alkalosis
­RR, resp acidosis, resp
fatigue, ARDS, hypoxia
Refractory hypoxemia, resp
failure
41
GI/GU/
hepatic
¯Hypoactive gut
¯UO, ­blood glucose,
­RAAS
¯ Absorption of nutrition,
GI bleeds, ATN; ­ LFTs;
insulin resistance
Gut failure, renal hepatic failure
Skin/
temp
Normal or febrile; warm
Hyperthemic ®
hypothermic
Hypothermic; mottled skin
Systemic Inflammatory Response Syndrome (SIRS)
• Presents like sepsis but can’t isolate infectious cause
• Generalized inflammation, not necessarily at initial site
• Treatment is the same: antibiotics and fluids
Multiple organ dysfunction syndrome (MODS)
• Failure of 2 or more organ systems
• Cannot maintain homeostasis
• All organs dysfunctional requiring mechanical support
• Neuro: non responsive; coma, Glasgow coma scale
• CV: vasoactive support, hypotension
• Hematology: platelet count decreasing
• Pulmonary: mechanical ventilator
• Renal: CRRT, serum creatinine, UO
• Liver: coagulopathies, hypoalbuminemia, serum bilirubin
• GI: not tolerate TF
• Skin: mottling
• Poor prognosis 70-80% mortality with 3+ system failures
• The care for MODS is to prevent and treat infection (if present), maintain tissue oxygenation, nutritional
and metabolic support, and support the individual failing organs.
Interprofessional Care
• Prevention is key! Assessment is important
• Quick intervention
• Specific numbers less important than the trends
• Sooner you recognize better survival
• Oxygen and ventilation
• Increase CO by fluid replacement
• Increase hemoglobin by whole or PRBC
• Supplemental oxygen
• High flow typically
• Mechanical ventilation
• Fluid resuscitation - Septic, hypovolemic & anaphylactic
• Large bore IV or central venous catheter (femoral, subclavian, jugular)
• Fluids - When large amounts of fluids are given make sure you monitor for hypothermia and
coagulopathy.
• Crystalloids (NS or hypertonic solutions)
• Colloids (albumin)
42
•
•
•
Blood products
• Hemoglobin <7-8
Improve perfusion
• Give drugs after adequate fluid resuscitation or for those who don’t respond to fluid
• Sympathomimetic drugs - Cause peripheral vasoconstriction
• Norepinephrine, dopamine, phenylephrine, vasopressin
• Increase SVR can harm patient in cardiogenic shock
• Goal MAP > 65mm HG
• Vasodilators - For cardiogenic shock to decrease afterload
• Nitroglycerin, nitroprusside,
• Prevention the harmful widespread vasoconstriction
• Goal MAP >65 mmHG
Nutrition
• High protein High caloric
• Enteral nutrition with 24 hours
• Parenteral if unable to meet at least 80% caloric requirements enterally
• Slow continuous drip
• Insulin drips in ICU to regulate blood sugar
• Insulin drips used to keep BS below 180
More Drugs used in Shock (Ionotropes)
They are medications that increase or decrease the force of muscular contraction. In the world of shock, we are
thinking of the heart muscle or arteries as what we want to alter.
+ Ionotropes
• Epinephrine
• Norepinephrine
• Isoproterenol
• Dopamine
• Dobutamine
• Digitalis
• Calcium
Negative Ionotropes
• Calcium channel blockers
• B-adrenergic blockers
• Clinical conditions (acidosis)
When do you use vasoactive drugs?
- vasoactive agents increase the afterload which means the heart will need to work harder to push blood out.
- Vasoactive agents could be used in shock but always remember before you give any vasoactive agent you
need volume, fluid in the vessels otherwise you are just clamping down on a vessel which will not help with
perfusion.
- These medications are all IV drips and are used in the intensive care unit.
- These drugs are titrated by the nurse using the MAP as a guide.
- Patients are also on a monitor while receiving these drugs.
- If someone is receiving very high doses of the drug you can see this in their skin or fingertips because of the
vessels clamping down so hard.
- Think about what this can mean to patients with DM or PVD.
o That said, saving a life is better than trying to preserve a few toes or fingers so again it is always
a risk benefit ratio.
43
Diagnostics for Septic Shock
- To diagnosis shock you need to monitor trends/values there isn’t 1 specific test that confirms shock.
- Lactic acid can determine an increase in anaerobic metabolism which is an indicator of shock.
- Hemodynamic monitoring can also be helpful, depending on how critical a patient is presenting.
o measurement of pressure, flow and oxygenation within the cardiovascular system.
o assesses heart function, fluid balance, and effects of interventions (fluids/meds) on CO.
o Invasive and non-invasive
Perfusion indicators Svo2/Scvo2
• This is indicated for the critically ill patient who has the potential to develop an imbalance between oxygen
supply and metabolic tissue demand like with sepsis, ARDS, or high-risk cardiac surgery.
• Placement
o Most central catheters are in the superior vena cava near the junction of the right atrium.
o Scvo2 is taken from the central venous catheter which is assessing blood from the superior
vena cava so it misses some of the venous return from the inferior vena cava.
o Svo2 is taken from the PA catheter
o This is truly a mixed oxygenation because it is getting a reading from both the inferior and
cardiac sinus vein which drains the blood from the myocardium into the right atrium.
o The heavily desaturated myocardial blood decreases the Svo2 for this reason.
44
•
One clinical rule of thumb is to subtract 30 from sao2 to get Svo2. If the Sao2= 100%-30%= 70% Svo2. You
will notice that the Scvo2 is higher than the Svo2 this is due to the location of the catheter
• Scvo2 =Central venous oxygen saturation
• Derived from central venous pressure with oximetric capability
• N=70-80% indicating a stable oxygen balance
• Svo2 = mixed venous oxygen saturation
• derived from the pulmonary arterial catheter
• N=60-80%
• If Svo2 or Scvo2 changes by more than 10% and is maintained for more than 10 minutes, then think
about these four factors:
• Arterial oxygen saturation
• Cardiac output
• Hemoglobin - level needs to be extremely low before changes in Scvo2/Svo2 are seen unless they
have a compromised cardiovascular system
• Oxygen consumption
• Implications
• As a critical care nurse, monitor for changes in Scvo2/Svo2 during routine nursing care and allow
the body to return to normal before doing another activity.
• Examples of things that could alter Scvo2/Svo2 could be turning, backrub, or getting a
patient out of bed.
Interprofessional Care: Cardiogenic shock
Most effective treatment of cardiogenic shock is coronary artery reperfusion
• Cardiac catheterization (initial)
• Angioplasty with stenting
• Valve replacement
• Vascular bypass
• Circulatory assist device
• Intra-aortic balloon pumping (IABP)
• Balloon on a catheter is positioned in descending thoracic aorta.
• Inflate during diastole to ­ coronary perfusion
• Deflates immediately before systole to ¯ afterload
• Assist with O2 delivery to heart and ­ contractility
• LVAD for people awaiting heart transplant
• IV rates restrictive
• Cardiac pain
• Morphine to reduce sympathetic stimulation caused by pain/anxiety
• which decrease cardiac workload and risk associated with catecholamines
• Decrease O2 consumption
• Sedation agents, address pain, calm environment,
• reduce fever
• Give blood, more oxygen, improve CO
• Goals of drug therapy: Dilating coronary arteries
• IV nitrates (dilate coronary arteries)
• Diuretics: ↓Preload: (lasix)
• Vasodilators: ↓afterload: (nipride, nitroglycerin)
• Betablockers: reduce rate, contractility
• Inotropic agents: contractility: Doba, Epi, Milrinone
45
Interprofessional Care: Hypovolemic Shock
Fluid resuscitation
• Stop fluid loss
• bleeding
• Fluid resuscitation is a 3:1 rule
• Blood products
• PRBCs, FFP, or platelets
• Watch for hypothermia bc shivering increases O2 demand
• 2 large bore peripheral IVs- central access if able
• May give calcium – important for clotting cascade
• Vasoactive drugs
• *FLUIDS GIVEN FIRST prior to so that there is volume in the intravascular space
Interprofessional Care: Septic Shock
• Large amounts of fluid replacement
• 30-50ml/kg with target CVP 8-12
• Vasopressors added
• Corticosteroids if not responding to fluids and vasopressors
• Obtain blood culture, antibiotics started early
• Frequent monitoring of blood glucose (<180 mg/dL)
• Stress ulcers
• Bundle from case study: R measure lactate, give fluid, get blood cultures, give antibiotics, and then give
vasopressors.
Interprofessional Care: Neurogenic Shock
• Stabilize spine*
• Vasopressors (phenylephrine)
• Atropine (bradycardia)
• Monitor for hypothermia
Interprofessional Care: Anaphylactic Shock
• First step is to prevention do a thorough
history
• IM Epinephrine is 1st drug of choice
• Causes peripheral vasoconstriction
and bronchodilation and opposes
histamine
• Adjunct Diphenhydramine and ranitidine
• Block the massive release of
histamine
• Patent airway
• Bronchodilators
• aerosolized epinephrine to treat
laryngeal edema
• Endotracheal intubation or cricothyroidotomy
Interprofessional Care: Obstructive Shock
• Mechanical decompression
• Pericardial tamponade
46
•
•
• Tension pneumothorax
• Hemopneumothorax
PE - Thrombolytic therapy
Abdominal - Decompressive laparotomy: compartment syndrome
Overall Summary
- Outcome is the same despite the cause
- Treat the cause
- Fluids and drugs except for cardiogenic shock
o Vasodilators and offload volume for cardiogenic shock
- With regard to BP, arterial blood pressure is considered the gold standard.
o BP serves as a warning that hemodynamics may be threatened, use this parameter in addition to
YOUR assessment of the patient for S/S of poor tissue perfusion
- Contractility
o With less resistance to flow (vasodilation), the myocardium is less stimulated to contract and
ejects with less force; BP drops and perfusion declines.
o With greater resistance (vasoconstriction), the heart contracts with more force (using more O2
and increasing workload). Vasoconstriction helps with BP, however, a critical point is reached
in which too much vasoconstriction occurs and the heart cannot overcome this resistance, and
CO falls.
o It’s all about finding the perfect balance!
Burn
Pathophysiology
1. Burn occurs
2. Pain
3. Inflammatory process (s/s – pain, heat, redness, swelling, loss of fxn)
a. More pain
b. Increased blood flow
c. Release of vasoactive substances
d. Increased capillary permeability
4. Fluid shifts (complications of fluid loss below)
a. Edema
b. Hypovolemia
c. Shock
d. Pain continues
e. Tissue and organ damage
5. Edema
6. Tissue and organ damage
7. Fluid mobilization and diuresis
8. Healing / Rehab OR…
9. Shock (tissue and organ damage continues)
Burn Classification
- By Etiology- Most common etiology: fire/flame and scald
• Increased home fire death rates for children and elderly
- Depth of tissue damage
- Total body surface area (TBSA) involved, and severity.
Etiology: Burn Types
47
-
Thermal: exposure to heat generating sources
o Forms: flame, steam, scald, hot objects/surfaces
o Inhalation injury: heated gases
Chemical: alkaline, acidic agents & organic compounds
Electrical: injury related to voltage
Radiation: usually from radiation therapy or exposure to industrial exposure (nuclear plants) covered in
Cancer
Other: conditions = loss of skin /epidermal cells
What is the role of the skin?
- Protective Barrier
- Sensation
- Water Balance
- Temperature Regulation
- Vitamin Production
- Cosmetic
Superficial Burns:
- Epidermal layer - outermost layer
- Common Cause: sunburn, minor
scalds
- S/S Mild erythema, hypersensitivity,
Blanches & painful
- Healing: few days (3-5); no scaring
- Complications: irritability &
discomfort
- No real medical intervention but…
o OTC- relief gel or cream;
Hydration: PO
o Common meds: NSAIDS:
Acetaminophen/Ibuprofen;
Diphenhydramine (Benadryl)
o Moisturize: No alcohol or
perfumes
Partial Thickness
- Injury: epidermis & minimal layers of
Dermis
o Various depths
- Appearance: Blisters, erythema, shiny,
wet, inflamed
o Cap refill time on blisters
remains WNL
- Pain: hypersensitivity r/t nerve injury;
extremely sensitive to touch and even to
air
- Mild to moderate edema
- May heal: 1-3 weeks
- Minimal to zero scar
48
-
But…without adequate perfusion burn damage can extend further into the dermis and convert to a deep
partial thickness burn (secondary injury)
Medical intervention:
o Treatments: designed to promote self-healing
o May require grafts
o Difficult to predict healing in “deep” partial thickness
o Blisters: “deroof” > 2cm
o Wound Care: Antimicrobial topical with non adherent dressings = daily wound care with
thorough cleansing
o Hydration: PO or IV (systemic)
o Optimize function: positioning
o Systemic Antibiotics:
§ if signs of infection present
§ Teach S/S infection - delayed healing, increase pain, increased exudate, purulent exudate
(Pus), redness, swelling
Deep Partial Thickness
- Injury: Epidermis and bottom layers of dermal tissue
o Hair follicles and sweat glands destroyed…
- S/S - Less moist, Decreased sensation & pain, light pink to cherry red
- Risk of conversion to full thickness
- Systemic fluid support - minimize conversion to deeper tissue injury
- Pain management: varying levels
- ñNutritional needs
- May require excision and skin grafting
- Assess and RX for maximum Function
- Risk for infection – takes longer to heal
Full Thickness
• Injury: all layers including portions of subcutaneous tissue
• May involve fat, muscle &/or bone
• Nerve damage = Non tender no pain, or no increase in pain when pressure is applied to wound
(aka insensate)
• Epidermal and dermal structures are destroyed, including hair follicles, sweat glands, and nerve
endings
• Burns that extend beyond the subcutaneous layer into muscle and/or bone are also considered
full thickness as seen in
• Causes: Contact, flame, scald burns, Electrical Burns, Intense or prolonged exposure
• S/S Non blanching, non-tender, dry, white, brown, black, tough & leathery, red, waxy (aka eschar);
usually do not form blister
• Do not heal on own - Requires excision and skin grafts
• Systemic fluid support
• Nutritional support
• Functional support/positioning
Depth of Burns
• Zone of coagulation:
• area that had the most contact with the heat source and severe damage.
• The tissue undergoes protein coagulation and eschar is often present, and the patient often reports no
pain within this area because all nerve cells are destroyed.
49
•
•
Zone of stasis immediately surrounds the zone of coagulation and is characterized by damaged cells and
impaired circulation
• At risk for conversion
Zone of hyperemia
• Area of increased blood flow
Burn Conversion: Inadequate resuscitation may cause the burn to become deeper because of limited blood
flow, causing the zone of stasis to convert into the zone of coagulation
Inhalation Trauma
- Consider in patients with facial burns, or Injury that occurs in an enclosed space; 20-50% of burn pts
admitted suffer inhalation injury
- Independent predictor of death
- Complications associated with carbon monoxide poisoning, injury above & below glottis
- Inhalation injury: increases incidence: Respiratory complications
- Complications
o Loss of cilia
o Respiratory epithelial cells
o Neutrophil infiltration
o Atelectasis: occlusion by debris
o Pseudomembranous CASTS
o Bacterial colonization@72 hr >> pneumonia
o ARDS
o Asphyxiation
Inhalation Depth
- Above Glottis
o More common
o Protective reflex
o Oral mucosa burns
o Lung parenchyma not injured
o Facial/airway edema primary nursing concern
- Below Glottis
o Patient possibly unconscious at the scene
o Injury to airway PLUS Injury lung parenchyma
o Complications: Atelectasis; pneumonia; ARDS; death
o Large % of those with injury below glottis require intubation
Types of Inhalation Trauma
- Carbon monoxide poisoning
o Inhalation: heated gases/smoke
o History of injury while in an enclosed space
- Carbon monoxide poisoning asphyxiation
o CO binds selectively to Hgb molecule ® hypoxia
o Treat with 100% FiO2
o injury in enclosed space; cherry red face
o Pulse ox considerations
Case Study: History of injury while in an enclosed space
- Primary Concern: Maintain Airway
50
-
-
o Facial burns
o Wheezing (47%)
o Carbonaceous sputum
o Rales
o Dyspnea; Tachypnea
o Hoarseness
o Cough
o Singed facial hair, nasal,
o Painful swallowing
Swelling greatest 2-96 hours
o Anticipate Intubation
o Early intubation 1-2 hrs post injury
o 6-12 hours bronchoscopy if not intubated Recheck airway
Airway patency: High Fowlers HOB > 45 -- No pillow
Suctioning (✓ carbon in sputum)
Maintain moist airway
Monitor/assess atelectasis, pulmonary edema, pneumonia, ARDS, infection
Electrical Injury
• Electrical energy converts to heat
• Current travels: path of least resistance
• Least: nerves, blood, fluid
• Most: bone, skin
• Majority of tissue destruction is “internal”
• Injuries are “hidden”
• Small surface injuries
• Devastating internal injuries
• Generated heat damages adjacent muscle and tissues
• Deep muscle & nerve injury may occur when superficial muscle appears normal
• Difficult to assess internal injury
• Medical Intervention
• Fluid resuscitation based on TBSA injury
• Identify contact points
• EKG-cardiac monitoring for 24 hours - Hyperkalemia, immediate threat to life in the hours
immediately after injury, occurs in 10-40%. Liberated potassium can cause life-threatening
dysrhythmias and death. Remember: K+ lives inside the cell when the cells are destroyed K+
leaks out = may cause hyperkalemia
• Assess: compartment syndrome with neurovascular checks q 1hr
• Detailed neurological exam q1hr - note changes over time
• Assess for rhabdomyolysis and myloglobinuria (ATN)
• Rhabdo: send labs: (cbc, chemistry, coag, lactate, troponin, CK, urine myoglobin
• Excess myoglobin may thus cause renal tubular obstruction, direct nephrotoxicity
(ischemia and tubular injury), intrarenal vasoconstriction, and acute kidney injury
(AKI) … (this is why the urine is dark red)
• Hypocalcemia occurs early in the course of rhabdomyolysis. Supplemental calcium is not
recommended.
• The BUN-creatinine must be monitored
• Goal: UOP to > 100 – 150 cc/hr
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High Voltage Injury
- Consequences/ Risk
- Loss of Consciousness
- Cardiac Arrhythmias
- Muscle contractions: Clenched fists
- Myoglobinuria: Product of Muscle breakdown
- Mummified extremities
Compartment Syndrome
- Increased pressure within body compartments
- Causing inadequate perfusion and inadequate nerve conduction
- Result is tissue and nerve necrosis beyond site of increased pressures
- Limb threatening and life threatening
- Generally found in full thickness circumferential burns or electrical burns, pt with large resuscitation
- Neurovascular assessment
o Sensation/ parasthesias
o Pulse checks: ≈15-60min
o Capillary refill checks
o General ‘feeling’ of limb
- Treatment: Escharotomy or fasciotomy
o Compartment pressures > 30mmHg
o Loss/decrease of sensation in extremity
o Loss of dopplerable pulses
o “Bovie” at the bedside or in OR
o Cuts: through inelastic eschar or into fascia
o Result: return of flow through/to body part à + pulses, + perfusion, + sensation
Common Chemical Burns
Acids
• Sulfuric - Car battery
• Sulfurous - bleach
• Hydrofluoric - polishes
• Acetic - Vinegar
Basic
• Lime-calcium oxide - cement
• Lye - Drain cleaners, air bags
• Magnesium hydroxide - Fireworks, flares
• Ammonia - cleaners
Chemical Burns
- Do not look for chemical antidote
- Do not try to neutralize chemical
- Protect yourself!
- Brush off any powder, remove clothing
- Irrigate: copious amounts of water
o Irrigation > 20 minutes
- Identify the causative agent
o without delaying patient care)
- Chemical burn alone meets referral criteria to a burn center
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Stevens Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TENS)
- Both Severe cutaneous hypersensitivity reactions
- Rash: exfoliative skin and mucous membranes
- Cause: Drug Reaction (50%)
o Antiepileptics (AED)
o Antibiotics: esp. sulfa, PCN
o Anti-gout meds
o Other rare
§ Vaccines
§ Infections
§ Grafts
- Difference: SJS < 10 TBSA & TENS > 30 % TBSA
- All Epidermal cells: skin & mucous membranes: eyes, mouth, GI, GU, peri areas
o Macules: Red, tender blisters coalesce, into blisters
- SJS: Mortality > equal size burn or 0-38%
- TENS Mortality 25-80%
- Sepsis is the most common cause of death
Frost Bite
- ED/EMS: Warm extremities slowly
§ Do not place in hot water.
§ Warm whole patient
- Tissue destruction from cold is like burns
- Depth of tissue damage:
§ Assessed when extremities are warm
and perfused
- Pain management (IV)
- Treatments:
§ Topicals: Antimicrobials OR allow
tissue to desiccate and mummify
§ Possible amputation
§ Some can heal without surgery
§ Refer to Burn Center within 24 hrs for
tPA
SYSTEMIC EFFECTS OF MAJOR BURN
INJURIES
- Burns: Less 20% TBSA produce a localized
tissue response.
- Burns: Greater than 20% TBSA are considered major injuries
- Produce both localized and systemic responses.
- All body systems are affected by the release of cytokines and other mediators into the systemic circulation.
To Measure – Rule of Nines and Lund Browder (more specific)
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Primary Survey Assessment: A, B, C, D, E
- Airway and C-spine stabilization
§ Maintain a patent airway (may require intubation- assess for inhalation injury )
• check if possible Advanced Directive/Code Status ….prior to ETT
§ Consider cervical spine immobilization if warranted
- Breathing
§ Provide high-flow 100% oxygen by mask
§ Assessment of burns and impact on work of breathing
- Circulation
§ Elevate extremities (no pillow under head)
§ Remove tight jewelry or clothing
§ Pulse checks with circumferential burns and electrical burns
- Disability - Neurological examination
- Expose and examine - Extent and depth of burn wounds and possible associated trauma
- Fluid resuscitation - Insert a minimum of two large-bore peripheral IVs and start lactated Ringer
Secondary Survey Assessment Includes:
- Circumstances of the injury
§ Cause? Exact time of injury? Enclosed space? Associated trauma (electrical)? Length of time
before rescue? Chemicals involved? Use of accelerant?
- Medical history, current medications, allergies, and vaccinations, Last food and fluid intake documentation
- Complete “head-to-toe” physical examination
- Determine the extent and depth of burn injury (calculate TBSA percentage)
- Cover the wounds with a clean, dry sheet
- Maintain core body temperature, pain medication, IV narcotics preferred
- Tetanus status and Initial laboratory values/tests: CBC, CMP, PT/aPTT, urinalysis, surveillance cultures,
ABG and carboxyhemoglobin level for suspected inhalation injury
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-
12-Lead ECG and CK-MB/troponin for electrical injury
Fluid resuscitation calculation and IV fluid rate adjustment
Types to go to burn center
- Chemical burns
- Partial thickness > 20% TBSA
- Deep partial thickness burns
- Lighting – electrical
- Burns at joint face, hands, feet, perineum
- Circumferential burns
- Frostbite
- SJS
Phases of interventions
- Emergent • first 48 hours
- Acute (intermediate) - weeks to months
- Rehabilitation >2 years
Burn Shock
- Hypovolemic & Distributive
- Massive fluid loss externally - heavy protein
loss
- Significant interstitial fluid shifts
§ Wound edema
§ Third spacing
Physiological Response to Burn Injury – Early
(Less than 48 Hours)
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Physiological Response to Burn Injury – Greater than 48 hours
Circulation
- Large fluid requirements to maintain tissue perfusion
- Under-resuscitation leads to an overwhelming acidosis
§ (Lactic acidosis)
- Over-resuscitation can increase complications
- lung injury, ARDS, compartment syndromes
- Optimize - Early and adequate resuscitation
- Resuscitation begins with the Parkland formula for resuscitation and the “rule of nines”
ABLS Recommendations for >30% TBSA Burns
Emergency Dept:
- Fluids are calculated via formula
- Foley catheter
- Temperature Control: at all stages of care
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Monitoring Perfusion During Resuscitation
- UOP out of target range for two consecutive hours
- increase or decrease fluids by 20% (or 1/3 depending on facility)
Example Calculation: Fluid Resuscitation
- 4 ml LR x TBSA x kg
- A patient has a 40% TBSA Thermal Burn; The patient weighs 80 kg
- How much fluid resuscitation does he need?
- 4 ml X 40 X 80 = 12,800 ml
- He needs ½ of this amount in the first 8 hours and the other half over 16 hours
- Needs 6,400 in first 8 hours: set pumps to deliver 800 ml / hour
- Needs 6400ml in following 16 hours: set pumps to deliver 400 ml/ hr
-
Monitoring Perfusion During Resuscitation:
- UOP out of target range for two consecutive hours increase or decrease fluids by 20%
Electrical Injury Fluid Resuscitation
- 4 ml LR x kg x TBSA burn
- Maintain urinary output at 75-150 ml/hour
- Monitor: goal may be up to 150/hr or higher
• Whatever is deemed necessary to clear
- May need to increase UOP to 1-1.5 ml per kg per hour to clear urine
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-
Rationale: protect kidney
Goals of Care – General
✔ Adequate gas exchange and respiratory pattern ✔ Adequate tissue perfusion ✔ Prevent extension of injury
- Extent of burn tissue injury cannot be fully assessed until 24 hours after burn
- Poor tissue perfusion in the first 24 hours can extend depth of burn
- Burn “converts” to deeper tissue injury This is a secondary injury
Airway – Breathing
- Assessment
- Facial burns, inhalation injury or burn >25% TBSA
- inhalation injury—early intubation
- Bronchoscopy- into airway: scope(see)/camera/suction
- Humidification of O2
- Essential to keep airways clear!
- Apply 100% 0xygen: removes CO; monitor carboxyhemogobin
- Assess: sputum: carbon, soot, thick or dry?
- Aggressive pulmonary interventions
- Monitor: Pulmonary edema, atelectasis, pneumonia, ARDS
- HOB elevated
Circulation
- Adequate tissue perfusion
- Cardiac concerns
- Hypovolemic shock - massive metabolic acidosis (tissue lactate)
- K+ released in massive amounts
• Monitor K+ & treat dysrhythmias
- Cardiac output increases complications
- IV access critical
• Central line - CLABSI bundles
- Hemodynamic markers: CVP > 10 and SV 70% or SVV < 13-15
- Urine output >30-50 hr
- ABG: Acidosis
• Lactate <2 mmol/L
• Base deficit (BE)
Emergent Phase
- Pain management
- Small, frequent doses, or infusion
- Sedation-anxiolytic
- GI symptom management
- NG
• Prevent & manage ileus
• Manage intubated patients
- Small bore feeding tube- placed early
• Feed within 24 hours; hypermetabolic injury
• Curling’s ulcer: stress ulcer
o H2 blocker, cytoprotective, PPI
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-
-
Thermal Control
- Cannot maintain temp
- Warming blankets
- High room temp
- Warming lamps
Infection control
- Gown and gloves for contact
- ALL wound care and at ALL times for burns >20% (@ UCH)
- Topicals
- High risk of Sepsis
Emergent Phase Summary
- 1st 48 (up to 72)
- Main Goals
• Perfusion
• Effective ventilation/oxygenation
• Pain management and emotional care
• Nutrition…. needs to get started
• Wound care not main priority until patient is stable
Acute Phase (72 hours to closure)
- Fluid Balance
- Edema Management
- Promote Wound Closure
- Goals: •Infection Prevention • Pain control •Adequate nutrition • Prevent complications
Wound Care
- Priority: once patient is stable
- Topicals •Antimicrobial Agents • Bacitracin • Silver sulfadiazine (Silvadene) • Sulfamylon: cream/soaks
- Enzymatic: Collagenase • enzymatic debridement)
- Medical Grade honey
- Antifungal: nystatin
- Hydrotherapy - Uses water to loosen dead tissue and assist with removal of tissue and agents & prevents
hypothermia
- Debridement: • Mechanical • Enzymatic • Surgical
- RN – monitors patients, administers anxiolytics and pain meds (high dose meds)
Types of Grafts
- Autograft: Patient’s own skin
- Allograft
- Cadaver skin
- Temporary covering
- Xenograft
- Pig skin
- Temporary covering
- CEA
- Cultured epithelial cells “grown” from small portion of skin
- Expensive
- Used when tissue can’t be taken from patient
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-
TBSA > 85%
Autograft Types: Sheet Graft vs. Mesh Graft (BOTH -- split thickness of pt’s own skin)
- Sheet Graft
- One continuous piece of skin
- better cosmetic outcome
- Used for faces, hands, feet, and joints
- Mesh Graft
- Holes or “interstices” are placed in harvested skin to increase the surface coverage area
- Covers larger areas of the body
Wound sites: Graft and Donor site
- Graft site:
- No pressure on site
- Roll out bubbles of air and fluid Keep edges moist
- Observe for “take”…usually 5-6 days
- Donor site
- Pain Management (New increased pain area)
- Moist to dry wound healing (think of a scab)
- Thin dressing
- Heals 7-14 days
Side BAR!
How to calculate MAP!!
Sx1+Dx2/3
Pain Management
- Hypermetabolism
- Patient: rapid metabolizing meds
- Higher dosing
- More frequent dosing needed
- Not addiction…
- More pain with each treatment bc nerves are regenerating
Meds –
- Beta blockers – Propranolol decreases energy expenditure
- Benzos
- Antidepressants
- Anabolic steroids – Oxadrolone (increases muscle protein metabolism)
- Growth hormone
- Assess hx of ETOH, MJ, amphetamines, etc.
Nutritional Concerns
- Hypermetabolic state > 2 yrs post injury
- TBSA > 40%= 2X resting metabolic rate
- Consumes nutrients
- Metabolizes drugs more quickly
- >20% need additional kcal
- Malnutrition primary concern
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-
High dose Vitamin C - decrease fluid needs and increase healing
MultiVit, Folic acid, Zinc
Protein & calorie rich diet
- 2-3g/per kg q 24 ° OR 15-25% of kcal from protein intake/24°
Enteral nutrition preferred vs TPN
Low fat High Carb
Post pyloric
Tube feeds: 24-hour goal and hourly goals used
- Accounts for hold periods
Burn Wound Infection
- Cellulitis
- Assess for erythema, edema, increased pain
- Will need debridement and possible IV antibiotics
- Will prevent the wound from healing
Rehab Phase
- Wound closed
- 80% tissue strength
- Itching
- Temperature regulation
- Longest stage—years
- Goals: • Mobility • Maximal function • Effective coping • Role resumption/ adaptation
Mobility
- Starts with first day in hospital
- ROM
- Positioning: splinting position of greatest function; keep extremities in extended position
- No pillows
- Scars constrict & decrease mobility
- Concern over joint spaces - contractures form
Skin
- Skin care/prevention
- Scar massage
- Scar compression – Elastic wraps – Pressure garments – Tight fitting – Skin stretch
- Cosmetic concerns for patients
- Compliance concerns
Fractional Ablation Laser Therapy
- LASER: Transformation of light into heat - Vaporizing old scar creating new wound with new healing
- Ablation: removal of target tissue
- New Remodeling
- Complications: Dry, peeling, itching, delayed hypopigmentation, infection
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