Type III Achalasia following Herpes Zoster Infection A Case Study A Common Syndrome with an Unusual Presentation Type III Achalasia following Herpes Zoster Infection Disclosure Relationships with commercial interest organizations whose products are related to the program content include ID: 935508
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A Case Study: A Common Syndrome with an Unusual Presentation: Type III Achalasia following Herpes Zoster Infection
A Case Study: A Common Syndrome with an Unusual Presentation: Type III Achalasia following Herpes Zoster Infection
Slide2Disclosure: Relationships with commercial interest organizations whose products are related to the program content include: None
Slide3Case SummaryA 75 year old patient presented with an erythematous band like rash in a dermatomal distribution to her right upper back, extending to her right lateral chest. She was diagnosed with shingles (Herpes Zoster), and discharged from the ER.Twelve days later, she was admitted with odynophagia and dysphagia to liquids and solids, and could not even tolerate sips of water. An EGD was performed and found to be normal.
Esophageal manometry was performed, showing significant high pressurization and esophageal spasm throughout the body of the esophagus, as well as failure of LES relaxation. The diagnosis was Type III achalasia.EGD with Botox to the LES was performed to provide temporary relief of symptomsTen days post Botox treatment the patient was tolerating a general diet, without symptoms of odynophagia or dysphagia.
Slide4The interest of this case study is to consider the uncommon presentation of shingles coinciding with Type III Achalasia.To understand the relationship of the two events, we have to consider: The Herpes virus The “Brain of the Gut” Immune Inflammatory Reactions
Achalasia
Slide5Chicken pox is caused by a single virus in the herpes family, known as Varicella Zoster Virus- VZVVaricella (chickenpox), develops when someone is exposed to VZV for the first timeVARICELLA
(CHICKENPOX)
Slide6Most people get chickenpox when exposed to someone else with chickenpox. VZV is very contagious, and can even be spread by direct contact. The virus can also spread when someone with the virus coughs or sneezes; tiny droplets carrying the virus are expelled and inhaled. The virus enters the lungs, then the bloodstream.
Slide7TheThe virus is then carried to the skin
Slide8Once the virus is carried to the skin, the characteristic chickenpox rash occurs. The rash consists of small itchy, fluid filled blisters occurring on the scalp, face and trunk before spreading to other parts of the body.
Slide9During the chickenpox episode, the Varicella virus migrates to nerve cells called dorsal root ganglia. www.unn.edu
Slide10When the virus reactivated, the disorder is called shingles, Herpes zoster. The virus spreads In the ganglion, and to the nerves connecting it to infect cells in the skin.
Herpes Zosterwww.nature.com
Slide11TheAnatomy of the esophagus
www.me240.eng.uci.eduThe esophagus functions to transport food and liquids between the UES and LES
Slide12Slide13PERISTALSISwww.slideplayer.com
Slide14www.slideshare.net
Slide15Swallowing initiates peristalsis
Peristaltic contractions start with the circular muscle and traverse the entire length of the esophagus
Slide16Lower Esophageal Sphincter
Slide17The Brain of the Gut: The Enteric Nervous System (ENS)The Enteric Nervous System (ENS), consists of 100 million neurons, that control gut function, including motility, absorption, and secretion.The Myenteric Plexus, a segment of the ENS, is a system of nerves (post ganglionic neurons) that innervating the esophageal wall and LES. This plexus “manages” esophageal motility.
Slide18Preganglionic neurons connect the CNS to ganglia
Postganglionic neurons connect ganglia to the effector organs
Slide19Excitatory neurons: Stimulation of the ENSExcitatory neurons in the plexus release acetylcholine Esophageal and LES contractions occur
Pennstatehershey.adam.com
Slide20Inhibitory Neurons: Inhibition of the ENSInhibitory neurons in the plexus release nitric oxide (NO) and vasoactive intestinal polypeptide (VIP)
Esophageal and LES relaxation occurwww.passmyexams.com
Slide21Interaction between excitatory and inhibitory neurons in the myentericplexus result in coordinated waves of peristalsis pushing food forwardInhibitory neurons are activated first to release nitric oxide, which relaxes the esophagus and allows for accommodation of the food bolus
www.clinicalgate.com
Slide22achalasia Achalasia is a motor disorder targeting the esophagus. It causes significant reduction in a person’s eating ability, and therefore can affect quality of life.Classic symptoms include progressive dysphagia to solids followed by liquids.
Slide23Causes of achalasiaAutoimmuneGenetic predisposition
ViralHerpes viruses exhibit a strong affinity for nerve fibers and can cause ganglion cell damage
Slide24Type 1 achalasiawww.mayoclinic.org
Failed peristalsisNo esophageal functionFailed LES relaxation
Slide25Type 2 achalasia
www.mayoclinic.orgNo peristalsisCompartmentalized pressurization for the entire length of the esophagusFailure of LES relaxation
Slide26Type 3 achalasia
www.mayoclinic.orgSpastic contractionFailure of LES relaxation
Slide27Type 3 achalasiawww.jamanetwork.c.com
Slide28Type 2 achalasia
www.memorangapp.com
Slide29Type 1 achalasia
www.memorangapp.comwww.mayoclinic.org
Slide30What about the immune system?Viral infections such a shingles cause an immune inflammatory reaction
www.everydayhealth.com
Slide31www.jonlieffmd.com
Slide32T lymphocytes are activated, that attack ganglion cells in the myenteric plexus of the esophagusThe inflammatory changes are associated with a decreased number of ganglion cells, and eventually tissue fibrosis
A consequence of this reaction is destruction of inhibitory neurons in the esophageal wall.Uptodate.com
Slide33Uptodate.comNerve fiber damage results in loss of inhibitory neurotransmitters NO and VIPResults are loss of esophageal peristalsis and failure of LES relaxation
Slide34conclusionIn this case study, it is probable the shingles infection triggered an immune-inflammatory response, resulting in significant affect in ganglion cell concentration in the myenteric plexus, specifically the inhibitory neurons. Loss of inhibitory neurons results in an imbalance; causing unopposed stimulation from excitatory neurons.The consequence of this process is loss of coordinated peristalsis in the body of the esophagus, and failure of LES relaxation.The effect on the inhibitory neurons in the myenteric plexus due to the virus is likely irreversible.
Slide35Failed relaxation of the LES
Pressurization in the body of the esophagus
Slide36Failed relaxation of LESHigh amplitude esophageal spasm
Slide37Local injection of Botox (Botulinum Toxin), was effective by counteracting the excessive LES tone. The Botox blocked the release of acetylcholine (excitatory neuron), allowing relaxation of the LES. Symptom relief is due to lowered LES pressure.
www.medlineplus247
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Striated muscle receives innervation directly from the vagus nerveSmooth muscle, including the LES, receive innervation from postganglionic fibers
Slide40treatment options for achalasiaPneumatic dilation
www.cddcfresno.com
Slide41HELLER MYOTOMYwww.nballian.gr
Slide42www.slideshare.net