STEP 7

1. Mengapa pada pasien terdapat keluhan sesak nafas yang hebat setelah meminum obat
antibiotik gol penicilin?
Allergens (or antigens) are presented to T-cells by Antigen-presenting cells (APCs) during
the sensitization phase of Type I hypersensitivity. T-cells then signal for stimulation of B-
cells to produce IgE antibodies, which bind to the Fc receptors on mast cells and
basophils. Subsequently, the free antigen induces the crosslinking of these mast cell and
basophil bound IgE antibodies. This results in the degranulation of the cells and the
release of histamine, proteolytic enzymes, and other mediators (i.e., prostaglandin,
cytokines, leukotrienes, platelet-activating factors, macrophage inflammatory proteins,
tryptase, etc.). As a result, there is increased vascular permeability, peripheral
vasodilation, and smooth muscle contraction, which can manifest to increased mucous
secretions, bronchospasm, abdominal cramping, rhinitis, and potentially hypovolemia
or hypoxia. Pulmonary edema or general edema can also occur due to fluid shifting into
interstitial space. Individuals can experience pruritis and local response of asthma or a
systemic response of anaphylaxis
Type I Hypersensitivity Reaction; Malak Abbas; Mohamed Moussa; Hassan Akel; 2020

2. Mengapa kedua kelopak mata didapatkan angioedema dan urtikaria diseluruh tubuh?
Angioedem dimana saja ? kenapa angio di mata urtikaria dikulit?
a. Urtikaria
Urticaria (hives) is a group of inflammatory disorders characterized by wheal and
flare type skin reactions (urtica, erythema) and pruritus resulting from the release of
histamine and other mediators by activated skin mast cells. Urticaria symptoms are
mast cell–dependent and their induction requires mast cell activation
(degranulation) by specific or nonspecific triggers. Mast cells are key effector cells in
the immune response. Specific triggers of mast cell degranulation include
stimulation of mast cell surface IgE by selected allergens or drugs as well as physical
stimuli (cold, friction, pressure) in physical urticaria disorders. Nonspecific triggers
such as stress are relevant to all urticaria disorders. In addition, modulators of mast
cell activation and/or degranulation (ambient temperature, alcoholic drinks, fever,
emotions, hyperthyroidism, and other endocrine factors) can modify the induction
of symptoms and the course of urticaria.
b. Angioedema
Angioedema is caused by a rapid increase in permeability of submucosal or
subcutaneous capillaries and post-capillary venules with localized plasma
extravasation. Most causes of angioedema are dependent upon the release of
either histamine or bradykinin.
Angioedema; Allen P Kaplan; 2008
Anaphylaxis; M Sánchez Borges; 2015

3. Mengapa didapatkan RR cepat, nafas cuping hidung, retraksi subcosta, stridor, fase
ekspirasi memanjang dan juga wheezing?
Anaphylaxis results when antigen-specific IgE is present on mast cells and a systemic
exposure to antigen occurs, cross-linking the IgE. This results in the simultaneous
degranulation of large numbers of mast cells. Mast cells contain histamine and other
vasoactive mediators. Their sudden release, due to either an IgE-mediated anaphylactic
reaction or a similar non-IgE-mediated reaction (referred to as an “anaphylactic”
reaction), results in a sudden drop in blood pressure and blood volume, flushing,
itching, and potentially respiratory compromise, bowel oedema, and potential death.
Compensatory tachycardia in response to hypotension is considered a characteristic
feature
Because of vasodilatation and increased vascular permeability, fluid loss into the
extravascular space occurs leading to hemoconcentration and hypovolemia, followed
by arterial hypotension and tachycardia. Direct cardiac symptoms include arrhythmia,
bradycardia or myocardial infarction.
Silbernagl,Lang; Atlas of Pathophysiology; 2000
Anaphylaxis: diagnosis and management; The Medical journal of Australia; 2006
Guideline for acute therapy and management of anaphylaxis; Allergo J Int; 2014

4. Mengapa kedua tungkai pasien di elevasikan ?

Tindakan pertama yang paling penting dilakukan menghadapi pasien dengan syok
anafilaktik adalah mengidentifikasi dan menghentikan kontak dengan alergen yang
diduga menyebabkan reaksi anafilaksis. Segera baringkan penderita pada alas yang
keras. Kaki diangkat lebih tinggi dari kepala untuk meningkatkan aliran darah balik
vena, dalam usaha memperbaiki curah jantung dan menaikkan tekanan darah.
Penatalaksanaan syok anafilaktik; vinoshalni jessenggar dr. I gusti putu sukrana
sidemen,span.kar

5. Mengapa didapatkan muntah dan nyeri abdomen ?

6. Apa interpretasi dari pemeriksaan fisik dan vital sign pada skenario ? diberikan alasanya
Silbernagl,Lang; Atlas of Pathophysiology; 2000

7. Apa saja macam macam faktor pencetus yang dapat mengakibatkan keluhan pada
skenario?
Montañez MI, Mayorga C, Bogas G, et al; Epidemiology, Mechanisms, and Diagnosis of Drug-
Induced Anaphylaxis; 2017

8. Bagaimana patofisiologi dari skenario? Dijadikan satu

9. Apa pertolongan pertama yang dilakukan pada skenario? ( dijawab ABCDE terlebih
dahulu)
10. Bagaimana tatalaksana dari skenario?
Patients with severe anaphylactic reactions require constant monitoring, as late
reactions including arrhythmias, myocardial ischemia, and respiratory failure may
manifest as late as 12 hours after the initial event. In terms of drug treatment, for
anaphylactic shock especially the administration of epinephrine (plus norepinephrine, if
necessary) and forced fluid replacement are required. In patients with bronchospasm,
ß-sympathomimetics and, as second-line treatment, glucocorticoids are indicated (as
they are in patients with delayed progressive symptoms). Histamine antagonists
suppress the histaminergic effects. 
a. Adrenaline
The most important drug in the acute therapy of anaphylaxis is adrenaline
(epinephrine). Through the activation of α- and β-adrenergic receptors, adrenaline
 functionally antagonises all of the important pathomechanisms of anaphylaxis by
vasoconstriction, reduction of vascular permeability, bronchodilatation, edema
reduction and positive inotropy in the heart. Administered intravenously, it shows
the fastest onset of action of all anaphylaxis drugs. In a patient not in need of
resuscitation, immediate intramuscular application of a dose of 0.3 to 0.5 mg
adrenaline (body weight range 30 to 50 kg) to the outer upper thigh is the drug
therapy of first-choice. Compared with intravenous application, the risk of severe
cardiac side effects is considerably lower. In case of no response, the injection can
be repeated every 5–10 minutes, depending on side effects. If the patient is
unstable or during resuscitation, i.e. in case of respiratory and/or circulatory arrest,
adrenaline should be applied intravenously. For this, a dilution of 1 mg adrenaline
in 10 ml NaCl 0.9 %, i.e. a solution of 0.1 mg/ml is administered, depending on
effects and side effects, under continuous control of circulatory parameters. A
continuous infusion of approx. 0.05–1 μg/kg/minute is equally effective. Control of
pulse and blood pressure is mandatory.
b. Oxygen
In case of manifest cardiovascular or pulmonary reactions, immediate supply of
oxygen via an oxygen mask with reservoir bag, is recommended. Administration of
high flow 100 % oxygen is recommended. A laryngeal mask or a laryngeal tube can
be helpful. Only in rare cases will endotracheal intubation by an experienced
physician (usually emergency physician, anaesthesiologist) become necessary.
c. Volume Substitution
An important pathophysiological aspect of anaphylaxis is the resulting hypovolemia
which is treated with adequate volume substitution. For severe anaphylactic
reactions, the supply of large amounts of fluid within a short time is necessary. This
can only be achieved through large-bore venous access. If intravenous access is not
possible, a special intra-osseous needle can be inserted preferably into the tibia. In
case of anaphylactic shock, a supply of 0.5–1 liters, and possibly up to 2–3 liters of
fluid — depending on the response — in a very short time is required for adults,
for children initially 20 ml/kg body weight.
d. Antihistamines H1 receptor antagonist
The only H1 antihistamines registered for intravenous application in the acute
treatment of anaphylaxis are the first-generation substances dimetindene (0.1
mg/kg bw) and clemastine (0.05 mg/ kg bw) with their well-known sedating side
effects. Officially the maximum licensed dose of oral antihistamines is
recommended.
Standl, Thomas et al; The Nomenclature, Definition and Distinction of Types of Shock; 2018
Guideline for acute therapy and management of anaphylaxis; Allergo J Int; 2014

11. Apa tujuan dokter memasang EKG dan pulse oximetri?

a. EKG
(ECG) monitoring to detect injury patterns and dysrhythmias. Electrocardiographic
(ECG) monitoring of all trauma patients is important. Dysrhythmias—including
unexplained tachycardia, atrial fibrillation, premature ventricular contractions, and
ST segment changes—can indicate blunt cardiac injury. Pulseless electrical activity
(PEA) can indicate cardiac tamponade, tension pneumothorax, and/or profound
hypovolemia. When bradycardia, aberrant conduction, and premature beats are
present, hypoxia and hypoperfusion should be suspected immediately. Extreme
hypothermia also produces dysrhythmias.
b. Pulse Oxymetri
Pulse oximetry is a valuable adjunct for monitoring oxygenation in injured patients.
A small sensor is placed on the finger, toe, earlobe, or another convenient place.
Most devices display pulse rate and oxygen saturation continuously. The relative
absorption of light by oxyhemoglobin (HbO) and deoxyhemoglobin is assessed by
measuring the amount of red and infrared light emerging from tissues traversed by
light rays and processed by the device, producing an oxygen saturation level. Pulse
oximetry does not measure the partial pressure of oxygen or carbon dioxide.
Quantitative measurement of these parameters occurs as soon as is practical and is
repeated periodically to establish trends. In addition, hemoglobin saturation from
the pulse oximeter should be compared with the value obtained from the ABG
analysis. Inconsistency indicates that one of the two determinations is in error.
Patients with severe anaphylactic reactions require constant monitoring, as late
reactions including arrhythmias, myocardial ischemia, and respiratory failure may
manifest as late as 12 hours after the initial event
Standl, Thomas et al; The Nomenclature, Definition and Distinction of Types of Shock; 2018