Educational Blog about Anesthesia, Intensive care and Pain management

Ludwig’s Angina

Ludwig’s Angina

Ludwig’s Angina

Definition and Causes:

A rapidly spreading cellulitis of the floor of the mouth that can be produced by any infection. It involves the submandibular, sublingual, and submental spaces.

-Gram-positive cocci (usually streptococci), Staphylococcus aureus, and Staphylococcus epidermidis are now the most common organisms, but sometimes gram-negative rods or anaerobes are responsible. In 50% of cases, more than one organism is isolated.

-It is frequently precipitated by a dental infection involving the second and third lower molars, but trauma may be contributory.

-The condition usually arises from the teeth, but tongue piercing with metal barbells has provided a novel source of infection.

-The frequency is generally decreasing, but there is now a higher incidence in patients with associated systemic diseases. Antibiotics and aggressive surgical treatment have dramatically improved the mortality rate.

-Airway management is controversial, airway compromise develops insidiously, but the actual obstruction is abrupt.

Preoperative Findings:

1. Bilateral submandibular swelling proceeds to brawny induration of the neck. Although the submandibular space is primarily involved in Ludwig’s angina, spread into adjacent fascial spaces may occur.

2. Elevation of the tongue caused by cellulitis of the floor of the mouth.

3. Dysphagia secondary to swelling, and trismus.

4. Gradual onset, or sudden, upper airway obstruction.

5. There is frequently an underlying systemic condition, such as DM, AIDS, or substance abuse.

6. Other complications include; bacteremia, aspiration, retropharyngeal abscess, empyema, mediastinitis, internal jugular vein thrombosis, and pericarditis.

7. Fever, leukocytosis, and increased ESR.

Anesthetic Problems:

1. Trismus, not necessarily relieved by muscle relaxants, may make oral intubation difficult or impossible.

2. Sudden total upper airway obstruction producing hypoxia.

3. Intravenous induction of anesthesia may be hazardous because it can result in apnea and an inability to maintain ventilation on a mask.

4. On a prolonged history of dental sepsis, sepsis may track down through the retropharyngeal space into the posterior mediastinum, requiring awake oral intubation, ventilatory support, and an eventual thoracotomy for a thoracic empyema.

Anesthetic Management:

1. Aggressive early treatment with antibiotics reduces airway problems and the need for surgical intervention.

2. Less severely affected patients may be managed by close observation but only provided that staff is available who can manage acute obstruction. Some argue the case for early tracheostomy.

3. Surgical drainage with or without tooth extraction.

4. Anesthesia for surgery in which there is trismus, but without compromise of the upper airway:

a) Awake fibreoptic nasal intubation but with facilities for emergency tracheostomy available.

b) Inhalation induction and laryngoscopy. If the trismus relaxes and the vocal cords can be seen, a neuromuscular blocker can be given.

c) Tracheostomy may be required in the presence of spreading edema.

5. Airway maintenance in the compromised airway:

-Signs of airway obstruction including; stridor, dyspnea, dysphagia, secretions, and deteriorating oxygen saturations, may indicate the need for rapid, active intervention. In these patients, sedative premedication should be avoided and a drying agent is given.

-If there is significant stridor, a tracheostomy under local anesthesia may be considered.

-Emergency cricothyroidotomy under local anesthesia has also been reported.

Chiari Malformations

 Chiari Malformations

Chiari Malformations


-The Chiari malformation is a term encompassing a range of hindbrain maldevelopments.

-Problems include underdevelopment of the cranial fossa and overcrowding of the normally developed hindbrain, the risks of descent of hindbrain structures below the foramen magnum, and intermittent obstruction to CSF outflow from the fourth ventricle.

-There may be a relatively high CSF pressure in the head and a relatively lower one in the spine.

Types of Chiari Malformations:

There are four types.

Type I:

-Downward herniation of cerebellar tonsils of at least 3–5 mm below the foramen magnum and hindbrain overcrowding results in direct compression of the tissue.

-Clinical symptoms thus relate to CSF disturbances and direct compression of nervous tissue; they include headaches, pseudotumor-like episodes, a syndrome resembling Meniere’s disease, lower cranial nerve signs, and spinal cord disturbances without syringomyelia.

-It is mostly seen in young adults.

Type II (Arnold–Chiari):

-It is the most important and includes; thoracolumbar myelomeningocele, hypoplasia of the posterior fossa, and displacement of the cerebellar vermis, brainstem, and fourth ventricle.

-It presents in infancy or early childhood.

Type III: rare

-Dilated the fourth ventricle with cervical meningomyelocele.

Type IV: rare

-Cerebellar hypoplasia.

Other abnormalities:

1. May be associated with syringomyelia or syringobulbia, other skeletal abnormalities of the skull base and cervical vertebrae, or myelomeningocele. Syringomyelia is the term for an expanding, longitudinal cystic cavity within the spinal cord. In the communicating variety, there is continuity between the syrinx and the CSF in the central canal.

2. May need decompression of foramen magnum or cervical spine.

3. Progressive hydrocephalus may occur which needs shunt surgery.

4. Obstructive sleep apnea.

5. Recurrent pulmonary aspiration.

6. May exhibit abnormal autonomic control.

7. Patients may present with respiratory arrest.

8. Sudden unexpected death may occur.

Anesthetic Problems:

1. Increased ICP may lead to coning.

2. Symptoms may start after a dural puncture.

3. Bolus injections into the epidural space may lead to ICP increases in susceptible individuals.

4. Sleep apnea may occur in Chiari type I.

5. Acute cardiovascular collapse secondary to inadvertent brainstem compression in an infant.

Anesthetic Management:

1. A careful history should be taken in a patient with a ventriculoperitoneal shunt, to check for any signs that it is nonfunctioning. If there is doubt, a referral to a neurosurgeon is indicated. This is particularly important if the notes are absent, there is poor history or lack of follow-up.

2. Try to prevent anything likely to increase ICP, such as coughing, or hypercarbia from heavy sedation or analgesia.

3. Avoid straining in labor. Epidural anesthesia for Cesarean section was performed in a patient with type I Chiari who had a previous difficult tracheal intubation. Small doses of local anesthetic should be titrated gradually, to avoid sudden distension of the epidural space or decreases in arterial pressure.

4. Spinal anesthesia should be avoided.

Budd–Chiari Syndrome

 Budd–Chiari Syndrome

Budd–Chiari Syndrome


-A syndrome caused by obstruction to the hepatic venous outflow and resulting in a clinical picture of hepatomegaly and portal hypertension. It may be secondary to hematological disorders, malignancy, oral contraceptives, heart failure, or constrictive pericarditis.

-The three main sites of obstruction are:

1-Inferior vena cava

2-Large hepatic veins

3-Small intrahepatic venules.

-The condition may be acute or chronic. Acute Budd–Chiari syndrome with hepatocyte necrosis may require urgent portosystemic, decompressive, surgical, or interventional radiological procedures.

-Untreated hepatic venous thrombosis usually results in progressive liver failure and death. Medical treatment is of little help, therefore shunt procedures or liver transplantation will be needed.

Preoperative Findings:

1. Abdominal pain and swelling are the commonest symptoms. Ascites and hepatomegaly will be present in the majority. Vomiting, splenomegaly, jaundice, or bleeding from esophageal varices may also occur. If the vena cava is involved there will be dependent edema.

2. Liver function abnormalities depend on the site and severity of the obstruction. A liver biopsy may show outflow obstruction, hepatic necrosis, and fibrosis.

3. Etiological factors include polycythemia, paroxysmal nocturnal hemoglobinuria, antiphospholipid syndrome, protein C deficiency, factor V Leiden, myeloproliferative disorders, and mechanical factors, such as webs and tumors. Hepatic venous thrombosis has been reported in association with ulcerative colitis, but in the patient described, iron deficiency had concealed an underlying polycythemia vera.

4. Treatment is aimed at the preservation of liver function and includes thrombolysis, angioplasty, stent placement, portacaval shunt, mesoatrial shunt, and liver transplantation.

Anesthetic Problems:

1. Hepatic function may be compromised.

2. Surgery may be required for portacaval or mesoatrial shunt or liver transplantation. This has been described in a patient with paroxysmal nocturnal hemoglobinuria.

3. Patients may present during pregnancy when the condition must be distinguished from HELLP syndrome and acute fatty necrosis of the liver. Antiphospholipid syndrome and preeclampsia in a primipara presented with Budd–Chiari syndrome from thrombosis of the right hepatic veins.

Thrombotic thrombocytopenic purpura resulted in postpartum hepatic venous thrombosis. Paroxysmal nocturnal hemoglobinuria has been associated with hemolytic crises and Budd–Chiari syndrome during pregnancy. Maternal deaths have been reported.

Anesthetic Management:

1. Hematological examination is important because, in the absence of mechanical causes for hepatic vein thrombosis, there is a high incidence of underlying hematological abnormalities; these include myeloproliferative disorders, and paroxysmal nocturnal hemoglobinuria, systemic lupus erythematosus, and antithrombin III deficiency.

2. Assessment of liver function, including coagulation.

3. Low-dose heparin infusion from the first postoperative day has been recommended, with subsequent low-dose aspirin and long-term anticoagulation to reduce the risks of graft thrombosis.

4. Liver transplantation will cure the inherited thrombophilias, for example, factor V Leiden, protein C and S, etc.

5. In a patient with paroxysmal nocturnal hemoglobinuria who developed Budd–Chiari syndrome, the resolution was achieved following bone marrow transplantation.

6. Pregnant patients with paroxysmal nocturnal hemoglobinuria should be carefully monitored for the onset of Budd–Chiari syndrome.