EMERGENCY IN INTERNAL MEDICINE
Nuzirwan Acang
Faculty Of Medicine
Islamic University Bandung
ميحرلا نمحرلا الله مسب
INTRODUCTION
Definition
-Emergensi Medicine is unforeseen
combination of circumstaces or resulting state that needss for immediate action
-An urgent need for assistance or
relieve
( CONTINU …..)
In order to quickly and accurately assess the patient's initial condition in an emergency department, it is necessary to do
a short history and systematic physical examination of the presence of:
- A : Airways - B : Breathing - C : Circulation - D : Disability
- E : Exposure/Environtment
AIRWAY
◆
Secure airway is first priority uses of airway obstruction
❏ Think of three areas
- airway lumen: foreign body, vomit - airway wall: edema, fractures
- external to wall: lax muscles
(tongue), expanding hematoma
BREATHING
• LOOK for mental status, chest movement, respiratory rate/effort, patient’s colour
• LISTEN for air escaping during exhalation,
sounds of obstruction (e.g. stridor), auscultate for breath sounds and symetry of air entry
• FEEL for the flow of air, chest wall for crepitus, flail segments and sucking chest wounds
• ASSESS tracheal position, neck veins, respiratory
distress, auscultation of all lung fields
CIRCULATION
❏ Check level of consciousness, skin colour, temperature, capillary refill
Check of blood pressure
❏ Check the pulse for rate and rhythm ❏ Stop major external bleeding
- apply direct pressure
- elevate profusely bleeding
- use tourniquet as last resort
DISABILITY
❏ assess level of consciousness by AVPU method (quick, rudimentary assessment)
A - ALERT
V - responds to VERBAL stimuli P - responds to PAINFUL stimuli U - UNRESPONSIVE
❏ size and reactivity of pupils
❏ movement of upper and lower
extremities
EXP OSURE / ENVIRONMENT
• ❏ undress patient completely
• ❏ essential to assess all areas for possible injury
• ❏ keep patient warm with a blanket;
avoid hypothermia
INITIAL MANAGEMENT
❖ When doing the initial assessment simultaneously, actions are taken to overcome the emergency that occurred
❖ Therapy is given in accordance
with the pathophysiology of the
emergency that occurred
Medication and Equipment
Emergency treatment room should be
equipped with equipments and a suitable range of medications, which reflect the anticipated emergencies in the patient
populations, the practitioners’ skills and the distance to the nearest emergency
department.
Equipment
Essential Medicatioon
ENDOCRINE EMERGENCIES
–Diabetic Keto Asidosis
–Thyroid Storm
DIABETIC KETO ACIDOSIS
( DKA )
INTRODUCTION
• Diabetic Ketoacidosis is an acute,
major, life-threatening complication of Diabetes.
• It mainly occurs in patients with Type 1 Diabetes but it is not uncommon in
some patients with Type 2 diabetes
DEFINITION
• DKA is an extreme metabolic state caused by insulin deficiency. It is Defined as an acute state of
severe uncontrolled diabetes associated with ketoacidosis that requires emergency
treatment.
• It is a state of absolute or relative insulin deficiency aggravated by ensuing
hyperglycemia, dehydration and acidosis- producing derangements in intermediary metabolism.
Incidence of D.M in Indonesia
•The report on the results of Basic Health Research (RISKESDAS) in 2018 by the Ministry of Health, an increase in the
prevalence of DM to 8.5%.
( EPIDEMIOLOGY )
( CONTINU …. )
• DKA accounts for 14% of all hospital admissions of patients with diabetes
• DKA is frequently observed in diagnosis of type 1 diabetes and often indicates this
diagnosis (3%).
• The incidence of DKA in developing countries is higher.
• It is far more common in young patients.
DIAGNOSIS
ADA (2009)
•Glucose> 13.9 mmol/L (250 mg/dl).
•Bicarbonate< 18mmol/L; pH< 7.3.
•Ketones positive result for urine or serum
ketones by nitroprusside reaction.
ETIOLOGY
• Inadequate insulin treatment or noncompliance.
• New onset diabetes (20-25%)
• Acute illness
• Infection (30 to 40%)
• CVA
• Acute Myocardial Infarction
• Acute Pancreatitis
▪ Drugs
• Clozapine or olanzapine
• Cocaine
PATHOPHYSIOLOGY
• DKA is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis and ketonuria.
• It usually occurs as a consequence of absolute or relative insulin deficiency that is
accompanied by an increase in counter-
regulatory hormones (i.e, glucagon, cortisol, growth hormone, epinephrine).
• This imbalance enhances hepatic, lipolysis and ketogenesis.
CLINICAL PRESENTATION:
• DKA usually evolves rapidly, over a 24 hour period.
• Earliest symptoms are polyuria, polydipsia and weight loss.
• Nausea, vomiting and abdominal pain are usually present.
• Malaise, generalized weakness and fatigability.
• As the duration of hyperglycemia progresses, neurologic symptoms, including lethargy, focal signs, and obtundation can develop Frank
coma is uncommon in DKA.
(CONTINU…….)
• Ill appearanc
• Respiration (Kussmaul).
• Dry mucous membranes, dry skin and decreased skin turgor.
• Characterstic ketotic breath odor.
• Tachycardia
• Hypotension
• Tachypnea
• Confusion
LABORATORIUM
• Blood test for glucose every 1-2 hour.
• Renal function test.
• Urine dipstick test (acetoacetate).
• Serum ketones (3-hydroxybetabutyrate).
• CBC.
• Anion gap.
• Osmolarity.
MANAGEMENT
• Correction of fluid loss with intravenous fluids.
• Correction of hyperglycemia with insulin.
• Correction of electrolyte disturbances, particularly potassium loss.
• Correction of acid-base balance.
• Treatment of concurrent infection, if
present.
CORRECTION OF FLUID LOSS
• It is a critical part of treating patients with DKA.
• Use of isotonic saline.
• 15-20mL/kg/hour for the first few hours.
• Recommended schedule:
• Administer 1-3 L during first hour.
• Administer 1 L during second hour.
• Administer 1 L during the following 2 hours.
• Administer 1 L every 4 hours, depending on the degree of dehydration and CVP.
• When patient becomes euvolemic, switch to 0.45% saline is recommended, particularly if hypernatremia exists.
INSULIN THERAPY
• Intravenous regular insulin preferred.
• Initiated with IV bolus of regular insulin
(0.1 units/kg) followed by continuous infusion of regular insulin of 0.1 units/kg/hour.
• SC route may be taken in uncomplicated DKA (0.3 U/kg then 0.2 U/kg one hour later).
• When serum glucose reaches 200 mg/dl, reduce insulin infusion to 0.02-0.03 U/kg/hour and switch the IV saline solution to dextrose in saline.
• Revert to SC insulin, after patient begins to eat (continue IV infusion simultaneously for 1 to 2 hours).
CORRECTION OF ACIDOSIS
• Bicarbonate therapy is a bone of contention among physicians and still remains a
controversial subject, as clear evidence of benefit is lacking.
• Bicarbonate therapy is only administered if the arterial pH is less than 6.9.
• 100 mEq of sodium bicarbonate in 400 mL sterile water is administered over two hours.
Repeat doses until pH rises above 7.0.
• Bicarbonate therapy has several potential harmful effects.
COMPLICATIONS
• CVA
• Myocardial Infarction
• DVT
• Acute gastric dilatation
• Erosive gastritis
• Respiratory distress
• Infection (UTI)
• Hypophosphatemia
• Mucormycosis
• CVA
Thyroid Storm
Intoduction
• Is a rare but potentially life-threatening complication of Graves' disease.
• Thyroid storm is also know as thyrotoxic
is an acute state of hyperthyroidism where all of the signs and symptoms are
exaggerated.
• It can be life threatening but with quick
response can be controlled and managed
Triggers
• Trauma
• Infection
• Surgery
Clinical Manifestation
The symptoms of hyperthyroidism are exaggerated and may include
significant tachycardia, hyperpyrexia, congestive heart failure, neurological compromise, and gastro-enterological or hepatic dysfunction.
Precipitating factor :
Surgery, trauma, infection or an iodine
load
Treatment
• Treatment is largely symptomatic and etiology dependent
• Look back at the treatments in your hyperthyroid module
• Think also about the body’s functioning and the exaggerated symptoms of
hyperthyroidism that would be manifested
during thyroid storm
( Continu …..)
Treatments directed at thyroid gland and hormones
• Inhibition of new hormone synthesis with Thioamide drugs such as PTU and
methimazole
• Inhibition of hormone release with Iodine
& potassium iodide (Lugol’s solution) &
Lithium carbonate
( Continu …..)
What the heck is Lugol’s solution?
• Also known as Lugol’s iodine, this oral solution is specifically indicated for
patient’s with thyroid storm or preoperatively for a patient with hyperthyroidism
• It is a mix of iodine, potassium iodide
and distilled water
( Continu …… )
Treatments directed at preventing hormone’s affects on the body
• Polythiouracil (PTU)
• Corticosteroids
• Beta blockers (most importantly Propanolol)
• Amiodarone
• Plasmapheresis
( Continu …. )
Treatments directed at maintaining homeostasis
• Hyperthermia: acetaminophen, cooling blankets
• Fluid and electrolyte replacement
• Vasopressors
• Digoxin & diuretics if appropriate
Treatment Summary
Overall Goal: Reduce circulation thyroid levels and control symptom
– Beta blockers; decreases adrenergic hyperactivity (sympathetic outflow)
– PTU (large amounts): prevents synthesis of the hormone
– Glucocorticoids: inhibit hormone production and decrease peripheral conversion from T4 to T3.
– Sodium iodide solution (Lugol’s solution): High levels of iodide will initially suppress release of thyroid hormone
– Treat cardiac symptoms, fever and hypertension
HYPERSENSITIVITY DISORDERS
ALLERGIC EMERGENCIES
ANAPHYLACTIC
➢ Definition
Serious life threatening allergic that is rapid in action and may cause death
➢ Etiology
Medications (antibiotics, aspirin,etc) Foods (eggs, nuts)
Blood prodects
Insects bite/stings
ETIOLOGY
Medication
❖ Antibiotics (especially parenteral penicillins and other ß-lactams , )
❖ Aspirin and nonsteroidal anti- inflammatory drugs
❖ intravenous (IV) contrast agents are the most frequent medications
associated with life-threatening
anaphylaxis .
(CONTINU …….)
– Foods
Peanuts, seafood, and wheat are the foods most frequently associated
with
life-threatening anaphylaxis.
Bronchospasm and asphyxia are the
most frequent mechanisms
– Stinging insects
ants, bees, hornets , and wasp
Fatal anaphylaxis can develop when a person with IgE antibodies induced by
a previous sting is stung again
A fatal reaction occurs within 10 to 15 minutes. Cardiovascular collapse is
the
most common mechanism
)CONTINU …….)
(CONTINU ….)
Antigens commonly implicated in anaphylactic shock include
Medications, such as:
• Stings
• Nuts, Shellfish, Milk, Eggs
• Penicillin
• ACE inhibitors, Aspirin
• Anaesthetic drugs
• Latex
tusssssssssss Mukosa mata, hidung trakt respiratotius
Trakt intestinalis
Ig. E
Mast cell Enzym—plasma
globulin Histamin SRS-A
a. Permeable kap b. Vasodilatasi
c. Konstraksi otot polos d. Akumulasi eusinofil
Kinin a. Permeable kapiler b. Vasodilatasi c. Tekanan darah d. Migrasi sel polimorf
a. Mata : konjungtivitis b. Hidung : sinusitis, rinore c. Larynx : edema
d. Paru : asma, bronkitis e. G.I Tr : Muntah, diare f. Kulit : urtikaria, edema
erupsi
a. Tekanan darah b. Takikardi
c. Syok d. anuri Port d entry of
antigen
Yang memproduksi
mediator
Efek farmakologi
Efek klinik
Sistemik
PATHOPHYSIOLOGY
CLINICAL MANIFESTATION
Clinical features of anaphylaxis can vary
considerably dependant on the route of exposure of the allergen (Jevon and Dimond, 2004).
(CONTINU ….)
Clinical manifestation
- wheezing, larynxs edema, bronchospasm
- hipotension, palpitation dan tachycardi
- pruritus, urticaria, angio-edema - sincops
- nausea, voiting
❖Onset of anaphylaxis is usually
sudden (i.e. within minutes of to an
allergen
(CONTINU ……….)
• Sudden onset and rapid progression of symptoms
• Life-threatening airway and/or
breathing and/or circulation problems
• Skin and/or mucosal changes (flushing, urticaria, angio oedema)
• There is often a history of anaphylaxis or severe allergic reaction, but it may be the first exposure to the allergen and
the first presentation.
SEVERE SYMPTOMS
One or more of the following:
– LUNG: Short of breath, wheeze, repetitive cough – HEART: Pale, blue, faint, weak pulse, dizzy,
confused
– THROAT: Tight, hoarse, trouble breathing /swallowing
– MOUTH: Obstructive swelling (tongue and/or lips) – SKIN: Many hives over body
MANAGEMENT
1. Place the patient on the back (or in a position of comfort if there is
respiratory distress and/or vomiting.
2. Elevate the lower extremities.
3. Administer adrenaline*
4. Assess circulation, airway, breathing, and mental status, skin, and other
visual indicators.
)CONTINU ……)
• Primary Treatment
- Adrenalin 1:1000, 0,3 cc S.C
- Tourniquite on proximal of injection
- Adrenalin can be repaeated 3X, every 15-30 mnt
-
Oxygen through the nose, 2-3 L/mnt
- Free the airway, Neck hiperexstention position
- Suction mucous and monitor vital sign - Start I.V with normal saline
- Corticosteroid and antihistamin is not first
line treament
Prevention
• Perform a complete history, especially allergic diseases such as urtikaria, exzeem, asma
bronchiale and others
• Do a skin test
• Prepare an injection table for ingredients to treat if anaphylactic reaction occurs, in
sequence, as adrenalin, corticosteroid,
antihistamin, infusion set, intravenus fluid
(normal saline)
•
ه ب َر ه هلِل ُدْمَحْلَا
نْي همَلاَعلْا
