Group 2 Nuñez,Refuerzo,Abalos,Almonte,Almuete

CASE STUDY NO.4

THE TELLTALE HEART

1. What are the major diagnostic considerations?

a. Dry skin: Those that experience anticholinergic toxicity may end up with very dry skin. While dry skin alone
is not usually indicative of a serious medical issue, dry skin accompanied by other symptoms on this list may
be a sign of anticholinergic syndrome.

b. Fever: Body temperature may increase upon ingestion of anticholinergic substances. This means that the
anticholinergic effect is potentially toxic to the individual. If you develop a fever, especially with some of these
other symptoms, it may be a sign to seek immediate medical attention.

c. Heart rate increase: An increase in heart rate is common among those experiencing toxicity from
anticholinergic drugs. If your heart rate increases upon ingestion of a particular drug, it is something that
needs to be medically supervised. In some cases of anticholinergic toxicity, a person’s heart rate increase may
lead to other serious problems.

d. High blood pressure: It is known that blood pressure may also increase during anticholinergic toxicity. If
blood pressure becomes abnormally high, this could lead to additional medical problems.

e. Pupil dilation: When ingested in large doses, anticholinergic agents lead to pupil dilation. If someone’s
pupils appear abnormally large and they’re also displaying many other prominent symptoms, anticholinergic
toxicity may be the culprit.

f. Reduced bowel sounds: Another sign of toxicity is that of reduced bowel sounds or inaudible sounds from
the abdominal region. Bowel sounds are most commonly associated with digestion of food and bowel
movements. Those ingesting toxic amounts of anticholinergics may discover that they lack bowel sounds.

g. Constipation: Those taking large amounts of anticholinergics may experience constipation. Being unable to
pass a bowel movement can be frustrating and may result in secondary symptoms such as a stomach ache. In
addition to frustration associated with being unable to pass a bowel movement, urinary retention may also be
prevalent.

h. Urinary retention: In addition to constipation, many people find that they are unable to completely empty
their bladder. This excess urinary retention is considered “acute” but can be highly uncomfortable for the
individual.

i. Seizures: seizures, coma and cardiovascular toxicity may not be mediated by muscarinic effects, rather
secondary to drug effects at other receptors, as many anticholinergic medications are active at numerous
receptors / ion channels.

j. Neurologic Examination: the patient responded to painful stimuli with symmetric decorticate posturing

k. Stupor: It is common for an individual experiencing anticholinergic toxicity. They may lack critical mental
function and a level of consciousness and is almost entirely unresponsive and only responds to base stimuli
such as pain. Those in a stuporous state are rigid, mute and only appear to be conscious, as the eyes are open
and follow surrounding objects.

REFERENCE:
Anticholinergic Toxicity: Causes, Symptoms, & Treatment. (2015, May 04). Retrieved from
https://mentalhealthdaily.com/2015/05/03/anticholinergic-toxicity-causes-symptoms-treatment/

2)What substances are capable of producing this syndrome?

The most obvious cause of anticholinergic toxicity is ingesting too much of an anticholinergic agent or multiple
anticholinergic agents. Anticholinergic toxicity is most likely to occur in the elderly taking anticholinergic drugs
due to the fact that most already have suboptimal levels of acetylcholine. In this case, adding a potent
anticholinergic to their medication regimen can result in dangerously low levels of acetylcholine.
 Anticholinergic agents: (Atropine, scopolamine,Glycopyrrolate,Benztropine, trihexyphenidyl)
There are hundreds of drugs and compounds that elicit anticholinergic effects within the body. This
includes prescription drugs, over-the-counter drugs, and even plants. If you are ingesting a large
amount of a drug with potent anticholinergic effects, you may be setting yourself up for a toxicity.
 Cold medicines: Various cold medications that you’re taking to treat runny nose, sinus drainage, and
congestion exhibit anticholinergic properties.
 Illicit drugs: Certain illicit street drugs like heroin are sometimes cut with large quantities of
anticholinergic agents like scopolamine. This can result in a quick toxicity that is difficult to identify.
 Plants: A variety of plants containing the belladonna alkaloid “atropine” elicit anticholinergic effects,
which may lead to anticholinergic toxicity.
 Atropa belladonna (deadly nightshade)
 Brugmansia spp.
 Datura suaveolens (angel's trumpet)
 Datura stramonium (jimson weed)
 Hyoscyamus niger (black henbane)
Mushrooms with anticholinergic properties include:
 Clitocybe spp.
 Inocybe spp

 Tricyclic antidepressants:(Amitriptyline,Amoxapine,Clomipramine,Desipramine,Doxepin,
Imipramine,Nortriptyline,Protriptyline)
This is an older generation of antidepressants that contain a three-ring chemical structure or “tricyclic”
bond. Tricyclic antidepressants often elicit significant anticholinergic effects that are believed to play a
role in their therapeutic efficacy.
 Sleep aids: Those taking sleep aids such as Doxylamine could result in anticholinergic toxicity,
especially if combined with anticholinergic medications.
In addition to anticholinergics, drug classes that have anticholinergic properties include antihistamines,
antipsychotics, antispasmodics, cyclic antidepressants, and mydriatics. Furthermore, several varieties of plants
and mushrooms contain anticholinergic substances.

 Antihistamines:(Chlorpheniramine,Cyproheptadine,Doxylamine,Hydroxyzine,Dimenhydrinate,Diphenh
ydramine,Meclizine,Promethazine)
 If you’re taking an antihistamine like Benadryl to reduce itchy skin or seasonal allergies, it is important
to realize that it acts as an anticholinergic. If you’re taking large amounts of over-the-counter
antihistamines, beware of potential toxicity.
 Antipsychotics with anticholinergic properties include the following:
 Chlorpromazine
 Clozapine
 Mesoridazine
 Olanzapine
 Quetiapine
 Thioridazine

 Antispasmodics with anticholinergic properties include the following:

 Clidinium
 Dicyclomine
 Hyoscyamine
 Oxybutynin
 Propantheline

 Mydriatics with anticholinergic properties include the following:

 Cyclopentolate
 Homatropine
 Tropicamide
 Miscellaneous drugs with anticholinergic properties include the following:
 Carbamazepine
 Cyclobenzaprine
 Orphenadrine

REFERENCES:
N.A.(N.A). Anticholinergic Toxicity: Causes, Symptoms, & Treatment.Retrieved
from:https://mentalhealthdaily.com/2015/05/03/anticholinergic-toxicity-causes-symptoms-treatment/
Mityanand,R.(2017). Anticholinergic Toxicity Clinical Presentation.Retrieved from:
https://emedicine.medscape.com/article/812644-clinical#b5

3. What drug may be given to confirm the diagnosis? What are the diagnostic and therapeutic indications
for its use?

Physostigmine salicylate
- Anticholinesterase

- Inhibit the enzyme choline esterase, which normally prevents excess accumulation of
acetylcholine, thereby increasing the level of naturally generated acetylcholine. Physostigmine is a tertiary
amine. For this reason, it is nonionized and lipophilic, and therefore it can rapidly cause the blood-brain
barrier to reverse central as well as peripheral toxic effects.

- The usual initial adult dose is 2 mg given slowly intravenously at 1 mg/min. A second dose of 1
to 2 mg may be attempted in 20 minutes if no reversal has occurred.
 - Specific indications for the use of physostigmine include the presence of one or more of the
following symptoms: convulsions, deep coma, severe agitations and hallucinations, hypertension, and
cardiac dysrhythmias.

- If the tentative diagnosis of cholinergic blockade is correct, and if the patient has not suffered
postanoxic brain damage or other additional insult, then the response is usually dramatic and rapid. One
must bear in mind, however, that the response can be attenuated or delayed if there has been ingestion of
combinations of drugs. Since physostigmine is rapidly metabolized, appropriate therapeutic doses of 1 to 4
mg may be necessary at 30 to 60 minute intervals to control life-threatening signs such as dysrhythmias,
convulsions, or deep coma. Repeated administration is risky, however, and it may result in cholinergic crisis,
including bradycardia, bronchospasm, hypersalivation, increased pulmonary secretions, and possibly
convulsions. Therefore a patient who is in an anticholinergic-induced coma but who is otherwise stable
should have physostigmine administered for diagnosis.

- If the diagnosis of cholinergic blockade is established, he should be managed with standard

supportive procedures as outlined below. If toxic cholinergic effects result from the physostigmine, then
atropine at one-half the dose of the previously administered physostigmine should be slowly administered.
Relative contraindications for the use of physostigmine include asthma, cardiovascular disease, gangrene
and mechanical obstruction of the gastrointestinal tract or the genitourinary tract.

REFERENCE:
Schneir, A. (2004). Physostigmine. California Poison Control System. Retrieved from
:https://calpoison.org/news/physostigmine
4. What additional diagnostic and therapeutic measures are indicated.
1. Administration of an Anti-Convulsant- The ambulance team reported that he had two generalized seizures
on the way to the hospital. We can say that the team, injected anti-convulsants to the patient to manage the
seizure. The anticholinergic syndrome is accompanied by seizures, coma, and cardiovascular toxicities.
2. Vital signs monitoring:
a. Blood Pressure- It was indicated that his blood pressure is 140/80mmHg. It is known that blood
pressure increases during an anticholinergic toxicity.
b. Pulse Rate- The patient’s pulse rate is reported 230/minute.
c. Respiratory Rate- The patient’s respiratory rate is reported 20/minute.
d. Temperature- The patient’s rectal temperature is reported 38.2 degrees Celsius. Body temperature
increases upon the ingestion of anticholinergic substances.
3. Inspection:
a. Pupils- Pupils were 6mm in diameter bilaterally, with minimal response to light. Fundi were benign.
b. Neck- The patient’s neck was supple.
c. Mouth- Mucus membranes of the patient’s mouth is dry and no abnormal odors are detected.
4. Percussion:
a. Bladder percussion- It was found to extend 4 cm above the pubic symphysis.
REFERENCE:
N.A(N.A).Diagnostic and therapeutic Considerations.Retrieved
from:https://fpnotebook.com/neuro/pharm/AntchlnrgcTxcty
 CASE STUDY NO. 5
THE NEAR-FATAL MISTAKE

1)What is the therapeutic regimen to be followed?

 In patients with caustic ingestion, airway monitoring and control is the first priority. When airway
compromise is present, a definitive airway must be established. In patients with a stable airway and no
clinical or radiological sign of perforation, medical therapy should be initiated.
 Arrangements should be made for urgent esophagogastroduodenoscopy (EGD) to grade the degree of
injury and establish long-term prognosis, In asymptomatic patients, however, EGD may be withheld in
favor of observation
 Emesis and gastric lavage are absolutely contraindicated in this patient. Emesis should be avoided
because of the potential for re-exposure of the airway to the caustic agent, which may result in edema
and airway compromise. Emesis may also result in bleeding or rupture of already-damaged tissues. The
insertion of an orogastric or nasogastric tube into the stomach for gastric lavage may also result in
perforation. There is no benefit to gastric decontamination since the caustic agents usually produce
their damage immediately on contact and there is little to no systemic toxicity associated with the
majority of these agents. pH-neutralizing solutions, such as dilute vinegar or bicarbonate are not
recommended because of the theoretical possibility of heat injury secondary to neutralization
reactions.
 Symptomatic and supportive measures
 Breathing support, including breathing tube
 Administer fluids by an intravenous drip line: Loss of fluid from the body due to severe
salivation may lead to loss of vital electrolytes, dehydration, and weaknesses
 Medications to treat severe pain(Intravenous Analgesic,NSAIDS,Opiods etc.)
 Esophageal burns- steroids
 H2 Blockers and antacids for 6-8 weeks-prevent reflux of acid in esophagus especially in
patients with injury in the mid or distal esophagus and stomach
 Esophageal or gastric perforation is treated with antibiotics and surgery
REFERENCES:
N.A.(N.A).Treatments for Chemical poisoning -- Clinitest tablet.Retrieved from:
http://www.rightdiagnosis.com/c/chemical_poisoning_clinitest_tablet/treatments.htm
Ksrdon,E.(2017). Caustic Ingestions Treatment & Management.Retrieved from :
https://emedicine.medscape.com/article/813772-treatment#d10
N.A.(2018). First Aid for Clinitest Tablets Poisoning.Retrieved from: https://www.dovemed.com/healthy-
living/first-aid/first-aid-clinitest-tablets-poisoning/
O’Malley, G.(2018). Caustic Ingestion.Retrieved from: https://www.msdmanuals.com/professional/injuries-
poisoning/poisoning/caustic-ingestion
2. What are corrosive burns?
Corrosive burns are chemical burn occurs when your skin or eyes come into contact with an irritant, such as an
acid or a base. Chemical burns are also known as caustic burns. They may cause a reaction on your skin or
within your body. These burns can affect your internal organs if chemicals are swallowed.
Your healthcare provider will make a diagnosis based on several factors. These may include: the level of pain
in the affected area, the amount of damage to the area, the depth of the burn, signs of possible infection, the
amount of swelling present.

3. What are some common corrosive agents? Where are they found, and who ingests them?

Examples:

 Acids

 Strong acids – the most common are sulfuric acid, nitric acid and hydrochloric acid (H2SO4,
HNO3 and HCl, respectively).
 Some concentrated weak acids, for example formic acid and acetic acid
 Strong Lewis acids such as anhydrous aluminum chloride and boron trifluoride
 Lewis acids with specific reactivity; e.g., solutions of zinc chloride
 Extremely strong acids (superacids)

 Bases

 Caustics or alkalis, such as sodium hydroxide, potassium hydroxide, and calcium hydroxide
 Alkali metals in the metallic form (e.g. elemental sodium), and hydrides of alkali and alkaline
earth metals, such as sodium hydride, function as strong bases and hydrate to give caustics
 Extremely strong bases (superbases) such as alkoxides, metal amides (e.g. sodium amide)
and organometallic bases such as butyllithium
 Some concentrated weak bases, such as ammonia when anhydrous or in a concentrated
solution

 Dehydrating agents such as concentrated sulfuric acid, phosphorus pentoxide, calcium oxide,
anhydrous zinc chloride, also elemental alkali metals
 Strong oxidizers such as concentrated hydrogen peroxide
 Electrophilic halogens: elemental fluorine, chlorine, bromine and iodine, and electrophilic salts such
as sodium hypochlorite or N-chloro compounds such as chloramine-T, halide ions are not corrosive, except
for fluoride
 Organic halides and organic acid halides such as acetyl chloride and benzyl chloroformate
 Acid anhydrides
 Alkylating agents such as dimethyl sulfate
 Some organic materials such as phenol ("carbolic acid")

Who?

 People who are at the highest risk for chemical burns are infants, older adults, and people with
disabilities. These groups may not be able to handle chemicals properly. You may be at increased risk
for chemical burns if you’re handling acids or other chemicals without assistance and you have
decreased mobility.
REFERENCES:
N.A.(N.A).Chemical Burns.Retrieved from:https://www.healthline.com/health/chemical-burn-or-
reaction#symptoms

N.A.(N.A.). Acid and chemical burns. Retrieved from:https://www.nhs.uk/conditions/acid-and-chemical-burns/

4. What are the characteristic aspects of caustic burns?

The pathophysiology of acid and base burns are distinctive. In acid burns the squamous epithelium of the
esophagus is usually relatively resistant, with typically a superficial mucosal reaction. Acids have their major
effects on the columnar epithelium of the stomach, leading to superficial corrosion and coagulation with
eschar formation. This eschar limits further penetration, thereby controlling the extent of the injury. In bases,
it typically produces a more severe injury known as liquefaction necrosis. This involves denaturing of proteins
as well as saponification of fats, which does not limit tissue penetration. If you swallow an alkaline chemical, it
will cause burns on the inside of your stomach. This may produce different symptoms than a chemical burn on
your skin.
In general, the common symptoms associated with chemical burns include:
 blackened or dead skin, which is mainly seen in chemical burns from acid
 irritation, redness, or burning in the affected area
 numbness or pain in the affected area
 a loss of vision or changes in vision if chemicals have come into contact with your eyes

The damage from a caustic burn:

 May extend through the entire epidermis and part of the dermis.
 It is characterized by redness and blisters.
 The deeper the burn the more prevalent the blisters, which increase in size during the hours
immediately following the injury.
 It may be extremely painful.
If caustic burns destroy the entire thickness of the skin:
 The surface of the wound is leathery and may be brown, tan, black, white, or red.
Some of the following symptoms may also occur if you’ve swallowed a chemical:
 irregular heartbeat
 headache
 low blood pressure
 cardiac arrest or heart attack
 shortness of breath
 coughing
 seizures
 dizziness
 muscle twitches

REFERENCES:

N.A.(N.A).Chemical Burns.Retrieved from:https://www.healthline.com/health/chemical-burn-or-reaction#risk-

factors
Cox,R.(2017).Chemical Burns.Retrieved from: https://emedicine.medscape.com/article/769336-overview#a7

5. What are the relationship among severity, location and outcome?

Severity of caustic injury depends on the location. Acids tend to affect the stomach more than the esophagus
because of the alkaline nature of oropharynx and the rapid transit of the acid through the esophagus.
However, the inability of gastric juices to neutralize acids contributes to the onset of lesions in various organs
such as the intestine. Nature of the location can also affect the severity for example presence of food in
stomach decrease the severity of caustic injury, as an empty stomach has no buffering or dilutional effect.

On the other hand Alkalis tend to affect the esophagus more than the stomach because esophagus is alkali in
nature and promote blood thrombosis in blood vessels by base absorption, impairing irrigation of the
esophagus. On the other hand alkali can be neutralized, at least in part, by gastric secretion, with a
consequent reduction of its action on the mucosa of the stomach. For this reason, acids usually provoke the
most severe lesions, especially in the antropyloric region. It should be remembered, however, that some
individuals have achlorhydria, a situation in which the destruction produced by alkali is quite extensive.
Similarly, since the esophagus has a slightly alkaline pH, its epithelium is resistant to acid, so that only 6 to 20%
of those who ingest this substance present lesions in this organ.

Severity and outcome of caustic damage have a direct relationship the higher the severity the worse the
outcome. And in relationship to the location it depends to the nature of the location. Other factors that may
contribute to the severity of caustic damage arequantity and concentration of the caustic substance ingested,
as well as on the time of contact with the mucosa.

REFERENCE:

Martins,R.et al.(2018). Ingestion of caustic substances and its complications Retrieved from
:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-31802001000100004

6. What is the clinical course of alkali induced esophagitis? What are the radiographic and endoscopic findings
in caustic esophagitis?

PATHOPHYSIOLOGY
 Caustic chemicals produce tissue injury by altering the ionized state and structure of molecules and
disrupting covalent bonds.
 Ingestion of caustic or corrosive agents causes acute and chronic inflammatory changes mostly in the distal
two-thirds of the esophagus. Whether the ingestion is accidental or intentional, the alkali agents penetrate
the layers of the esophagus and cause severe liquefaction necrosis.
 There are three characteristic phases of injury in caustic esophagitis: 1) acute necrosis, 2) ulceration-
granulation, 3) stricture formation.
 Patients will present with rapid onset of odynophagia, chest pain, vomiting, and hematemesis.

ALKALINE INGESTIONS
 Alkaline ingestions cause tissue injury by liquefactive necrosis, a process that involves saponification of fats
and solubilization of proteins. Cell death occurs from emulsification and disruption of cellular membranes.
The hydroxide ion of the alkaline agent reacts with tissue collagen and causes it to swell and shorten. Small
vessel thrombosis and heat production occurs. Severe injury occurs rapidly after alkaline ingestion, within
 minutes of contact. The most severely injured tissues are those that first contact the alkali, which is the
squamous epithelial cells of the oropharynx, hypopharynx, and esophagus.
 The esophagus is the most commonly involved organ with the stomach much less frequently involved after
alkaline ingestions. Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress
sufficiently to create airway obstruction. Over time, if the injury was severe enough, granulation tissue starts
to replace necrotic tissue.

RADIOLOGICAL FINDINGS
 Chest films may reveal a dilated esophagus or evidence of esophageal perforation.
 Abdominal films may show pneumoperitoneum secondary to gastric perforation.
 In the acute phase, esophagrams may show abnormal esophageal motility with diffuse spasms and poor
primary peristalsis.
 On double contrast studies, shallow ulcers may appear as punctuate, linear, or serpiginous collections of
barium.
 In severe cases, the esophagus may show diffuse narrowing with an irregular contour.
 Chronically, cicatrisation and fibrosis may lead to the development of strictures 1 to 3 months after the
injury. The strictures typically appear as areas of smooth, tapered narrowing in the cervical or upper thoracic
esophagus.

ENDOSCOPIC GRADING
Grade I: edema and erythema
Grade IIA: Hemorrhages, erosions, blisters, superficial ulcer, exudates (patchy or linear)
Grade IIB: Circumferential lesions
Grade IIIA: Small scattered areas of necrosis.
Grade IIIB: Multiple deep brownish-black or gray ulcers with extensive necrosis.
Grade IV: Perforation

REFERENCES:
Kardon, E. M. (2017). Caustic Ingestions. Retrieved May 6, 2018 from
https://emedicine.medscape.com/article/813772-overview
NA. (2013). Gastrointestinal Radiology: Corrosive/Caustic Esophagitis. Retrieved May 6, 2018 from
https://www.med-ed.virginia.edu/courses/rad/gi/esophagus/esophagitis04.html

Sudarsi, B. (2015). Clinical and Endoscopic Study of Upper GI Manifestation in Corrosive Acid Ingestion.
International Journal of Scientific and Research Publications, Vol 5, Iss 2. Retrieved May 6, 2018 from
https://www.ijsrp.org/research-paper-0215/ijsrp-p3884.pdf

7. What is a Clinitest tablet, and what are the complications of its ingestion?
Clinitest tablets are used to test how much sugar (glucose) there is in a person's urine. Clinitest tablets used to
check how well a person's diabetes was being controlled. These tablets are rarely used today. They are not
meant to be swallowed, but could be taken by accident, since they look like pills. Poisoning occurs from
swallowing these tablets.

Complications of ingesting Clinitest tablet:

 Blood in urine
 Burns and burning pain in the mouth, throat, and esophagus
 Collapse
 Convulsions
  Diarrhea, may be watery or bloody
 Lightheadedness
 Low blood pressure
 No urine output
 Pain during a bowel movement
 Severe abdominal pain
 Throat swelling (causes breathing trouble)
 Vomiting
 Weakness

REFERENCE:
-n.a. (n.d.) Clinitest tablets poisoning. Retrieved from
http://slu.adam.com/content.aspx?productId=117&pid=1&gid=002611

8. Are there any new modalities for treating these accidents?

Therapeutic considerations and recent advancements in treatment of caustic ingestion injuries:
a.) A controlled study suggested that a 3-day course of high-dose intravenous methylprednisolone might
reduce the occurrence of esophageal stricture (an abnormal narrowing of a body passage, especially a tube or
a canal) formation.

b.) Balloon dilatation has been shown to be as effective as other bougienage techniques with lower risk of
perforations. Bougienage is a procedure involving the use of a bougie, a thin cylinder of rubber, plastic, metal
or another material that a physician inserts into or through a body passageway, such as the esophagus, to
widen or guide another instrument into a passageway.

c.) Esophageal dilatation can be safely performed as early as 5-15 days after initial ingestion and may decrease
risk for long-term stricture formation.

d.) The use of adjunctive treatment, such as topical Mitomycin C and esophageal stents, reduces the
reoccurrence of stricture formation after dilatation.

REFERENCES:
-n.a (n.d.) Therapy of caustic ingestion: new treatment considerations. Retrieved from
https://www.ncbi.nlm.nih.gov/pubmed/26196260
-n.a. (n.d.) Medical Definition of Bougienage. Retrieved from
https://www.medicinenet.com/script/main/art.asp?articlekey=12535