Cocaine-induced Midline Destructive Lesion Research Articles

Cocaine- and Levamisole-Induced Vasculitis: Defining the Spectrum of Autoimmune Manifestations.

Drug-induced or associated vasculitis is a prevalent form of vasculitis that resembles primary idiopathic antineutrophil cytoplasmic autoantibody (ANCA) vasculitis (AAV). Cocaine is a diffuse psychostimulant drug and levamisole is a synthetic compound used to cut cocaine. Their abuse may result in a spectrum of autoimmune manifestations which could be categorized into three overlapping clinical pictures: cocaine-induced midline destructive lesion (CIMDL), levamisole-adulterated cocaine (LAC) vasculopathy/vasculitis, and cocaine-induced vasculitis (CIV). The mechanisms by which cocaine use leads to disorders resembling AAV are not well understood. Cocaine can cause autoimmune manifestations ranging from localized nasal lesions to systemic diseases, with neutrophils playing a key role through NETosis and ANCA development, which exacerbates immune responses and tissue damage. Diagnosing and treating these conditions becomes challenging when cocaine and levamisole abuse is not suspected, due to the differences and overlaps in clinical, diagnostic, therapeutic, and prognostic aspects compared to primary idiopathic vasculitides.

Complete Clival Resorption and Pontine Pneumatosis Secondary to Severe Cocaine-Induced Midline Destructive Lesion: A Case Report

BACKGROUND AND IMPORTANCE: Cocaine-induced midline destructive lesions manifest as various degrees of distortion to normal anatomy. We present a rare case of substance-induced clival defect that underwent surgical repair. CLINICAL PRESENTATION: This patient presented with transient neurological deficits and was found to have severe clival destruction and pontine pneumatosis secondary to prolonged cocaine use. Surgical reconstruction of the clival defect was performed using a combined open and endoscopic approach. DISCUSSION: When anatomical integrity is severely compromised, defects of the clival region can be repaired using a hybrid open-endoscopic approach. In this case, the lack of local mucosal tissue for reconstruction led to the use of a pedicled pericranial flap. CONCLUSION: Complete clival resorption secondary to cocaine use is uncommon. In advanced cases, pontine inflammation is present on imaging studies. Combined endoscopic and open clival reconstruction is effective in restoring anatomic integrity.

Oral Rehabilitation for a Patient with Cocaine‐Induced Midline Destructive Lesions

Background. Cocaine is the second most consumed drug worldwide, more than 0.4% of the global population, and has become a real public health problem in recent years. Its inhalation causes significant centrofacial lesions, grouped under the name cocaine‐induced midline destructive lesion (CIMDL). These destructions are due to the conjunction of the vasoconstrictor, local prothrombogenic effects, and cytotoxic effects of cocaine. The ischemia produced by this substance is due to vasoconstriction that leads to nasal tissue necrosis and perforation of the nasal septum secondary to chondral necrosis. Case Presentation. A 36‐year‐old man, previously grappling with cocaine addiction, was hospitalized to undergo comprehensive clinical, microbiological, and radiological examinations because he was suffering from the emergence of crusts and ulceration in the nasal mucosa, accompanied by a palate perforation, a 39°C fever, and chills. Standard bacteriological culture was positive for coagulase‐negative staphylococci and Escherichia coli, while mycological culture was positive for Candida tropicalis. The CT scan images of the sinuses confirmed the presence of palatal perforation and total destruction of the nasal septum, cartilaginous portion, maxillary sinus medial wall, lower and middle turbinates, and middle meatus. Nasal endoscopy revealed an exposition of the bony wall and displayed the exposition of the occipital bone’s clivus. A diagnosis of CIMDL was confirmed. Antibiotic therapy was decided based on antibiogram results by the consulting microbiologist. Debridement of necrotic tissue was done by nasal endoscopy with local cleaning and was repetitive during the first week to maintain the best cleanliness possible. The patient was discharged with oro‐nasal hygiene instructions and referred for prosthetic rehabilation. As for the cocaine addiction, the patient was in follow‐up with a psychologist in a specialized centre. Conclusion. The care is multidisciplinary. Psychological help and assistance are essential to guide patients to become cocaine free and to avoid a relapse. Weaning is a prerequisite for surgery. Rehabilitation of speech and swallowing is necessary. Many local flaps or micro‐anastomoses are possible.

The clinical manifestations of cocaine-induced midline destructive lesion: a real challenge for maxillo-facial surgeons, mapping evidence review

article: The clinical manifestations of cocaine-induced midline destructive lesion: a real challenge for maxillo-facial surgeons, mapping evidence review - Chirurgia 2022 December;35(6):317-28 - Minerva Medica - Journals

Focal Chronic Meningitis With Lymphoid Follicle-Like Structures Associated With Cocaine-Induced Midline Destructive Lesion: A Case Report

Focal Chronic Meningitis With Lymphoid Follicle-Like Structures Associated With Cocaine-Induced Midline Destructive Lesion: A Case Report

COCAINE-INDUCED MIDLINE DESTRUCTIVE LESIONS: TWO CASE REPORTS

BACKGROUNDChronic cocaine insufflation contributes to progressive damage of the sino-nasal mucosa. This is primarily attributed to the potent vasoconstrictive properties of cocaine, producing ischemic necrosis. In a small percentage of cocaine abusers, these damages culminate in the destruction of osteocartilagenous structures of the nasal cavity. The most common manifestations are nasal septal perforation, palatal perforation, and lateral nasal wall destruction involving the nasal turbinates. When at least 2 of these manifestations are detected, the diagnosis of a cocaine-induced midline destructive lesion (CIMDL) should be considered in the potential etiology.CASE REPORTMost CIMDL lesions are asymptomatic, limited in extent, and incidentally detected. We present 2 cases of asymptomatic CIMDLs first recognized as incidental findings on cone beam computed tomography (CBCT) scans. Both cases presented with nasal septal perforation and varying degrees of lateral wall erosion of the nasal turbinates. The medical histories did not include prior surgeries or pathologic conditions that could account for these midline lesions. On further inquiry, the patients admitted to chronic recreational use of cocaine.DISCUSSION/CONCLUSIONSThe radiologic appearance of CIMDL mimics granulomatosis with polyangiitis. In granulomatosis with polyangiitis, sino-nasal symptoms are present in almost all affected individuals and are often the first manifestations of the disease. Moreover, soft tissue nodules often accompany any osseocartilaginous destruction. Other inflammatory diseases, infectious diseases, and neoplasms may also have similar manifestations. Therefore, attributing midline destructive lesions to cocaine use is challenging yet paramount given the variety of possible etiologies and the potential implications for patient care. However, patients are often reluctant to disclose a history of recreational drug use. The disclosure of cocaine use is essential to establish the correct diagnosis and to avoid unnecessary or inappropriate diagnostic testing. Nevertheless, in the absence of cocaine use, a thorough medical examination and appropriate laboratory tests will be necessary to rule out other etiologies. Chronic cocaine insufflation contributes to progressive damage of the sino-nasal mucosa. This is primarily attributed to the potent vasoconstrictive properties of cocaine, producing ischemic necrosis. In a small percentage of cocaine abusers, these damages culminate in the destruction of osteocartilagenous structures of the nasal cavity. The most common manifestations are nasal septal perforation, palatal perforation, and lateral nasal wall destruction involving the nasal turbinates. When at least 2 of these manifestations are detected, the diagnosis of a cocaine-induced midline destructive lesion (CIMDL) should be considered in the potential etiology. Most CIMDL lesions are asymptomatic, limited in extent, and incidentally detected. We present 2 cases of asymptomatic CIMDLs first recognized as incidental findings on cone beam computed tomography (CBCT) scans. Both cases presented with nasal septal perforation and varying degrees of lateral wall erosion of the nasal turbinates. The medical histories did not include prior surgeries or pathologic conditions that could account for these midline lesions. On further inquiry, the patients admitted to chronic recreational use of cocaine. The radiologic appearance of CIMDL mimics granulomatosis with polyangiitis. In granulomatosis with polyangiitis, sino-nasal symptoms are present in almost all affected individuals and are often the first manifestations of the disease. Moreover, soft tissue nodules often accompany any osseocartilaginous destruction. Other inflammatory diseases, infectious diseases, and neoplasms may also have similar manifestations. Therefore, attributing midline destructive lesions to cocaine use is challenging yet paramount given the variety of possible etiologies and the potential implications for patient care. However, patients are often reluctant to disclose a history of recreational drug use. The disclosure of cocaine use is essential to establish the correct diagnosis and to avoid unnecessary or inappropriate diagnostic testing. Nevertheless, in the absence of cocaine use, a thorough medical examination and appropriate laboratory tests will be necessary to rule out other etiologies.

A case series and literature review on patients with rhinological complications secondary to the use of cocaine and levamisole.

Levamisole is an increasingly common cutting agent used with cocaine. Both cocaine and levamisole can have local and systemic effects on patients. A retrospective case series was conducted of patients with a cocaine-induced midline destructive lesion or levamisole-induced vasculitis, who presented to a Dundee hospital or the practice of a single surgeon in Paisley, from April 2016 to April 2019. A literature review on the topic was also carried out. Nine patients from the two centres were identified. One patient appeared to have levamisole-induced vasculitis, with raised proteinase 3, perinuclear antineutrophil cytoplasmic antibodies positivity and arthralgia which improved on systemic steroids. The other eight patients had features of a cocaine-induced midline destructive lesion. As the use of cocaine increases, ENT surgeons will see more of the complications associated with it. This paper highlights some of the diagnostic issues and proposes a management strategy as a guide to this complex patient group. Often, multidisciplinary management is needed.

Management of a cocaine-induced palatal perforation with a nasal septal button

A cocaine-induced midline destructive lesion (CIMDL) is a rare consequence of cocaine insufflation that involves the nose, sinuses, and occasionally the palate. Palatal perforations compromise swallowing, mastication, and speech. An obturator prosthesis can be used to overcome these complications. In selected cases, a nasal septal button is a good alternative for the sealing of a palatal perforation, especially when surgery is not indicated, such as in cases of persistent cocaine abuse. Abstinence from cocaine is the most effective long-term management option for patients with a CIMDL, and surgical correction of the defect should be postponed until the patient stops sniffing cocaine and the lesion becomes stable. We describe the case of a 39-year-old cocaine abuser whose oronasal communication was plugged with a nasal septal button, which resulted in an immediate alleviation of his oronasal reflux.

Oronasal Fistula with Palatal Involvement Secondary to Cocaine Use

Vasoconstriction is a well-known local sympathetic effect of cocaine that may lead to ischemia, inflammation, ulceration and ultimately necrosis of the nasopharyngeal structures implicated by snorting cocaine. 2 Nasal septal perforation is present in 4.8% of abusers, making it the most common complication of cocaine abuse. 3 Chronic cocaine use may contribute to larger lesions and further destruction of the surrounding osteocartilaginous structures. Specifically, the destruction of nasal and midfacial bones and soft tissues can lead to a syndrome called cocaine-induced midline destructive lesion (CIMDL). The diagnosis of CIMDL requires at least 2 of the following clinical or radiologic findings: nasal septal perforation, lateral nasal wall destruction, and hard palate involvement. 4 We describe a patient with a history of cocaine abuse and signs of CIMDL, with midfacial destruction of the nasal septum and hard palate creating an oronasal fistula. To the best of our knowledge, we believe this is the first case of CIMDL with oronasal fistula reported in Canada. case presentation A 60-year-old male was referred to us with a 1-month history of a “hole” in his hard palate that caused fluids to leak out of his nose when drinking. Prior to presentation, he had been using denture adhesive gel as a temporizing measure for the palatal defect. He also disclosed that he had a nasal deformity, which previous physicians had attributed to his long history of cocaine snorting. The oral and nasal lesions were not associated with bleeding, pain, B-symptoms, nasal obstruction or recurrent sinusitis. His past medical history was notable for asthma and hypertension. His social history revealed a lifetime of tobacco use and many years of chronic cocaine use. On physical examination, the patient looked well and was in no acute distress. The nasal vestibules were intact bilaterally with no erosion of the columellar skin. Anterior rhinoscopy revealed complete loss of the cartilaginous nasal septum, without saddle nose deformity. Flexible nasopharyngoscopy showed extensive mucosal crusting, severe atrophy of the turbinates bilaterally but no polyps or suspicious growths. Examination of the oral cavity showed normal mucosa and dentition overall, with a single 1 cm perforation at the midline of the hard palate, communicating with the floor of the nasal cavity. The hard palate was quite soft in the area surrounding the perforation, suggesting bone loss of 2‐3 cm in circumference. The soft palate was intact and the posterior pharynx was normal, with no ulcerating or fungating growths. The remainder of the head and neck examination was unremarkable. Computed tomography (CT) scan showed extensive bony erosion of the nasal septum and hard palate, with mucosal thickening of the maxillary and ethmoid sinuses. There was no evidence of orbital or intracranial extension of this disease. Nasopharyngeal swab was positive for Staphylococcus aureus. Biopsy of the nasal cavity mucosa showed non-specific granulation tissue with no evidence of malignancy or infection.

Repair of Cocaine-Related Oronasal Fistula With Forearm Radial Free Flap

Cocaine snorting may cause significant local ischemic necrosis and the destruction of nasal and midfacial bones and soft tissues, leading to the development of a syndrome called cocaine-induced midline destructive lesion. A review of the English-language literature reveals only a few articles describing the treatment of hard and/or soft palatal perforation related to cocaine inhalation. Described here are 4 patients with a history of cocaine abuse showing palatal lesions. From 2010 to 2013, a total of 4 patients affected by cocaine-related midline destructive lesions were referred to our department. They all presented signs of a cocaine-induced midline destructive lesion. They showed wide midfacial destruction involving the nasal septum as well as the hard and soft palates causing an ample oronasal communication. In 3 patients, oronasal communication has been treated successfully using a personal technique based on a partially de-epithelialized forearm free flap. The fourth patient had been treated only with local debridement because, when she came to our attention, her abusive habits were still unsolved. Different surgical options have been reported such as local, regional, and free flaps for hard and soft palate reconstruction. However, because of an unpredictable vascularization of the palatal tissues and owing to the scarceness of the local soft tissues, local flaps are at high risk for partial and complete failure. The transfer of free vascularized tissue, however, seems to be the most reliable and logical solution for medium- to large-sized fistulas. Among the various free flaps, we choose the radial forearm type because of the pedicle length and the flap thickness.

The manifestation of cocaine-induced midline destructive lesion in bone tissue and its identification in human skeletal remains

Cocaine-induced midline destructive lesion (CIMDL) is a condition that may arise in response to chronic insufflation (“snorting”) of cocaine. It is clinically diagnosed when the nasal septum, lateral nasal walls, and/or hard palate show signs of destruction in association with cocaine use. Although its true incidence is unknown, CIMDL is not an uncommon clinical finding amongst intranasal cocaine abusers and is likely to be encountered by forensic anthropologists and medical examiners working worldwide. Given the preponderance of drug abusers amongst the subjects of forensic casework, the ability to diagnose CIMDL in dry bone may provide crucial insight into an investigation and even help confirm an individual identification.This paper aims to make practicing forensic anthropologists aware of CIMDL. Through the analysis of existing clinical literature, patient CT scans, and histology sections, it works toward the establishment of formal diagnostic criteria for identifying CIMDL in human skeletal remains. Lytic destruction regularly involves the vomer and frequently extends to the perpendicular plate of the ethmoid, the palatal process of the maxillae or the palatine bones, and the inferior nasal conchae. The middle nasal conchae, medial walls of the maxillary sinuses, ethmoid sinuses, and cribriform plate are often damaged. Destruction may also implicate the superior nasal conchae, the orbit, and the sphenoid. Bones affected by CIMDL may contain necrotic lesions or may be absent entirely. Lesions show minimal, if any, signs of repair. The author proposes that this lack of new bone formation may be mediated by potentially elevated leptin levels in cocaine abusers and CIMDL patients and may be the key to differentiating CIMDL from other lytic processes of the midface.

Cocaine-Induced Midline Destructive Lesion and Wegener Granulomatosis

Cocaine-Induced Midline Destructive Lesion and Wegener Granulomatosis

A Case of Levamisole-Induced Systemic Vasculitis and Cocaine-Induced Midline Destructive Lesion

We describe a case of antineutrophil cytoplasmic antibody-positive vasculitis from levamisole-tainted cocaine with concomitant cocaine-induced midline destructive lesions of the palate and nasal septum. The diagnosis was confirmed after extensive clinical, laboratory, pathologic, and radiographic testing. Timely recognition of this clinical entity is critical to avoid misdiagnosis and unnecessary treatment with potentially harmful cytotoxic agents. Given the high rate of levamisole contamination within the nation's cocaine supply, clinicians should be alerted to this emerging health threat.

A 44‐year‐old woman with cutaneous bullae and extensive skin necrosis

Five weeks before presentation, the patient had experi-enced a cough and mild dyspnea. She was diagnosed withpneumonia, completed a 7-day course of ciprofloxacin anddoxycycline, and her respiratory symptoms resolved.Three weeks before presentation, the patient had reportedfevers, chills, diaphoresis, arthralgias, and myalgias, anddeveloped a small erythematous lesion on her left breast.The lesion subsequently enlarged and became hemor-rhagic. She simultaneously developed additional lesionson her chest, abdomen, arms, and back. The largest ofthese, located on her left arm, was 15 cm in diameter. Allof the lesions were exquisitely tender. She was hospital-ized at an outside hospital for 5 days and given a diagnosisof cocaine-induced vasculitis. Upon discharge, she wasinstructed to abstain from cocaine and was prescribedtrimethoprim/sulfamethoxazole for a possible cellulitis in-volving the skin lesions.Ten days after discharge from the outside hospital, thepatient presented to our institution for pain managementand further evaluation. The rash had progressed since herearlier discharge. She had continued to use cocaine, her-oin, and prescription opioids. She had last smoked co-caine 3 days before presentation and last used intranasalheroin 1 week before admission. She reported acquiringcocaine from a new supplier 2 weeks before her rash hadbegun.

Diagnostic considerations and prosthetic rehabilitation of a cocaine-induced midline destructive lesion: A clinical report

The intranasal inhalation of cocaine has numerous complications. In addition to its systemic effects, cocaine can cause extensive destruction of the osteocartilaginous midline structures of the palate, nose, and sinuses. Without an accurate social and clinical history, a cocaine-induced midline destructive lesion can cause diagnostic difficulties, because its clinical presentation closely mimics other diseases. This clinical report describes an oronasal defect caused by cocaine use, the diagnostic considerations of these lesions, and prosthetic management of the defect.

Cocaine-induced midline destructive lesion

Conflict of interest: none declared. Cocaine‐induced midline destructive lesion (CIMDL) is the term used to describe destruction of the osteocartilaginous structures of the nose, sinuses and palate caused by cocaine inhalation. The clinical appearance may mimic a vasculitis but it lacks the typical histopathological findings of a true vasculitis. This condition is often overlooked in clinical practice particularly if a history of cocaine inhalation is not sought or volunteered. It is vital to recognize this clinical condition to prevent immunosuppressive therapy being prescribed for a presumed vasculitis. A 29‐year‐old man was referred from the ear, nose and throat department with an 8‐week history of nasal swelling and ulceration associated with an episode of severe epistaxis (Fig. 1). He gave a 3‐year history of cocaine inhalation. Before his presentation, he had increased the frequency of his cocaine use. He was otherwise well, on no regular medication and had no family history of skin, sinus or joint disease.

A peculiar case of midface reconstruction with four free flaps in a cocaine-addicted patient

Cocaine-induced lesions may cause extensive destruction of the osteocartilaginous structures of the nose, sinuses and palate, a syndrome called CIMDL (cocaine-induced midline destructive lesion). In such cases, reconstructive procedures of the lost soft and hard tissues may be indicated, such as local flaps, regional flaps, and free revascularised flaps. Also, prosthetic obturators have been suggested to overcome the functional problems related to the tissue loss. However, the majority of publications are related to relatively small defects, whereas articles related to the surgical treatment of large midfacial defects are less frequently reported. The objective of this article is to report the authors' experience concerning a unique case consisting of a complex reconstruction of a severe cranial base, midface, palate, and nose defect following cocaine abuse with four revascularised flaps followed by prosthetic restoration with implant-supported prostheses.

Cocaine-related syndrome and palatal reconstruction: report of a series of cases

Intranasal cocaine abuse may cause significant local ischaemic necrosis and destruction of the nasal and midfacial bones and soft tissue, leading to development of a cocaine-induced midline destructive lesion. Review of the English-language literature reveals only a few case reports describing hard and/or soft palatal perforation related to cocaine inhalation. To date, among the reconstructive techniques of the palate, different surgical options have been reported such as local, regional and free flaps. Common prosthetic obturators have also been used. Presented here are six cases of cocaine abuse showing different types of cocaine-related palatal lesions treated with different surgical approaches including local and free flaps. Mean follow-up was 3 years. A surgical variation of Marshall's classic technique for insetting a free flap in such lesions is proposed.