NEET MDS Synopsis
Dens in Dente
PedodonticsDens in Dente (Tooth Within a Tooth)
Dens in dente, also known as "tooth within a tooth," is a developmental
dental anomaly characterized by an invagination of the enamel and dentin,
resulting in a tooth structure that resembles a tooth inside another tooth. This
condition can affect both primary and permanent teeth.
Diagnosis
Radiographic Verification:
The diagnosis of dens in dente is confirmed through radiographic
examination. Radiographs will typically show the characteristic
invagination, which may appear as a radiolucent area within the tooth
structure.
Characteristics
Developmental Anomaly:
Dens in dente is described as a lingual invagination of the enamel,
which can lead to various complications, including pulp exposure,
caries, and periapical pathology.
Occurrence:
This condition can occur in both primary and permanent teeth,
although it is most commonly observed in the permanent dentition.
Commonly Affected Teeth
Permanent Maxillary Lateral Incisors:
Dens in dente is most frequently seen in the permanent maxillary
lateral incisors. The presence of deep lingual pits in these teeth
should raise suspicion for this condition.
Unusual Cases:
There have been reports of dens invaginatus occurring in unusual
locations, including:
Mandibular primary canine
Maxillary primary central incisor
Mandibular second primary molar
Genetic Considerations
Inheritance Pattern:
The condition may exhibit an autosomal dominant inheritance pattern,
as evidenced by the occurrence of dens in dente within the same family,
where some members have the condition while others present with deep
lingual pits.
Variable Expressivity and Incomplete Penetrance:
The variability in expression of the condition among family members
suggests that it may have incomplete penetrance, meaning not all
individuals with the genetic predisposition will express the phenotype.
Clinical Implications
Management:
Early diagnosis and management are crucial to prevent complications
associated with dens in dente, such as pulpitis or abscess formation.
Treatment may involve restorative procedures or endodontic therapy,
depending on the severity of the invagination and the health of the
pulp.
HAEMORRHAGIC DISORDERS
General Pathology
HAEMORRHAGIC DISORDERS
Normal homeostasis depends on
-Capillary integrity and tissue support.
- Platelets; number and function
(a) For integrity of capillary endothelium and platelet plug by adhesion and aggregation
(b) Vasoactive substances for vasoconstriction
(c) Platelet factor for coagulation.
(d) clot retraction.
- Fibrinolytic system(mainly Plasmin) : which keeps the coagulatian system in check.
Coagulation disorders
These may be factors :
Deficiency .of factors
Genetic.
Vitamin K deficiency.
Liver disease.
Secondary to disseminated intravascular coagulation.or defibrinatian
Overactive fibrinolytic system.
Inhibitors of the factars (immune, acquired).
Anticoagulant therapy as in myocardial infarctian.
Haemophilia. Genetic disease transmitted as X linked recessive trait. Comman in Europe. Defect in fcatorVII Haemophilia A .or in fact .or IX-Haemaphilia B (rarer).
Features:
May manifest in infancy or later.
Severity depends on degree of deficiency.
Persistant woundbleeding.
Easy Bruising with Haemotoma formation
Nose bleed , arthrosis, abdominal pain with fever and leucocytosis
Prognosis is good with prevention of trauma and-transfusion of Fresh blood or fTesh plasma except for danger of developing immune inhibitors.
Von Willebrand's disease. Capillary fragility and decreased factor VIII (due to deficient stimulatory factor). It is transmitted in an autosomal dominant manner both. Sexes affected equally
Vitamin K Deficiency. Vitamin K is needed for synthesis of factor II,VII,IX and X.
Deficiency maybe due to:
Obstructive jaundice.
Steatorrhoea.
Gut sterilisation by antibiotics.
Liver disease results in :
Deficient synthesis of factor I II, V, Vll, IX and X Incseased fibrinolysis (as liver is the site of detoxification of activators ).
Defibrination syndrome. occurs when factors are depleted due to disseminated .intravascular coagulation (DIC). It is initiated by endothelial damage or tissue factor entering the circulation.
Causes
Obstetric accidents, especially amniotic fluid embolism. Septicaemia. .
Hypersensitivity reactions.
Disseminated malignancy.
Snake bite.
Vascular defects :
(Non thrombocytopenic purpura).
Acquired :
Simple purpura a seen in women. It is probably endocrinal
Senile parpura in old people due to reduced tissue support to vessels
Allergic or toxic damage to endothelium due to Infections like Typhoid Septicemia
Col!agen diseases.
Scurvy
Uraemia damage to endothelium (platelet defects).
Drugs like aspirin. tranquillisers, Streptomvcin pencillin etc.
Henoc schonlien purpura Widespeard vasculitis due to hypersensitivity to bacteria or foodstuff
It manifests as :
Pulrpurric rashes.
Arthralgia.
Abdominal pain.
Nephritis and haematuria.
Hereditary :
(a) Haemhoragic telangieclasia. Spider like tortous vessels which bleed easily. There are disseminated lesions in skin, mucosa and viscera.
(b) Hereditary capillary fragilily similar to the vascular component of von Willbrand’s disease
.(c) Ehler Danlos Syndrome which is a connective tissue defect with skin, vascular and joint manifestations.
Platelet defects
These may be :
(I) Qualitative thromboasthenia and thrombocytopathy.
(2) Thrombocytopenia :Reduction in number.
(a) Primary or idiopathic thrombocytopenic purpura.
(b) Secondary to :
(i) Drugs especially sedormid
(ii) Leukaemias
(iii) Aplastic-anaemia.
Idiopathic thrombocytopenic purpura (ITP). Commoner in young females.
Manifests as :
Acute self limiting type.
Chronic recurring type.
Features:
(i) Spontaneous bleeding and easy bruisability
(ii)Skin (petechiae), mucus membrane (epistaxis) lesions and sometimes visceral lesions involving any organ.
Thrombocytopenia with abnormal forms of platelets.
Marrow shows increased megakaryocytes with immature forms,
vacuolation, and lack of platelet budding.
Pathogenesis:
hypersensitivity to infective agent in acute type.
Plasma thrombocytopenic factor ( Antibody in nature) in chronic type
Chronic myelocytic leukaemia
General Pathology
Chronic myelocytic leukaemia
Commoner in adults (except the Juvenile type)
Features:
- Anaemia.
- Massive splenomegaly
- Bleeding tendencies.
- Sternal tenderness.
- Gout and skin manifestations
Blood picture:
- Marked leucocytosis of 50,-1000,000 cu.mm, often more
- Immature cells of the series with 20-50 % myelocytes
- Blasts form upto 5-10% of cells
- Basophils may be increased
- Leuocyte alkaline phosphate is reduced
- Anaemia with reticutosis and nucleated RBC
- Platelets initially high levels may fall later if patient goes into blast crisis.
Bone marrow:
- Hyper cellular marrow.
- Myeloid hyperplasia with more of immature forms, persominatly myelocytes.
Chromosomal finding. Philadelphia (Phi) chromosome is positive adult cases .It is a short chromosome due to deletion of long arm of chromosome 22 (translocated to no.9),
Juvenile type :- This is Ph1 negative has more nodal enlargement and has a worse prognosis, with a greater proneness to infections and haemorrhage
PNEUMONIAS
General Pathology
PNEUMONIAS
Pneumonia is defined as acute inflammation of the lung parenchyma distal to the terminal bronchioles which consist of the respiratory bronchiole, alveolar ducts, alveolar sacs and alveoli. The terms 'pneumonia' and 'pneumonitis' are often used synonymously for inflammation of the lungs, while 'consolidation' (meaning solidification) is the term used for macroscopic and radiologic appearance of the lungs in pneumonia.
PATHOGENESIS.
The microorganisms gain entry into the lungs by one of the following four routes:
1. Inhalation of the microbes.
2. Aspiration of organisms.
3. Haematogenous spread from a distant focus.
4. Direct spread from an adjoining site of infection.
Failure of defense mechanisms and presence of certain predisposing factors result in pneumonias.
These conditions are as under:
1. Altered consciousness.
2. Depressed cough and glottic reflexes.
3. Impaired mucociliary transport.
4. Impaired alveolar macrophage function.
5. Endobronchial obstruction.
6. Leucocyte dysfunctions.
CLASSIFICATION. On the basis of the anatomic part of the lung parenchyma involved, pneumonias are traditionally classified into 3 main types:
1. Lobar pneumonia.
2. Bronchopneumonia (or Lobular pneumonia).
3. Interstitial pneumonia.
BACTERIAL PNEUMONIA
Bacterial infection of the lung parenchyma is the most common cause of pneumonia or consolidation of one or both the lungs. Two types of acute bacterial pneumonias are distinguished—lobar pneumonia and broncho-lobular pneumonia, each with distinct etiologic agent and morphologic changes.
1. Lobar Pneumonia
Lobar pneumonia is an acute bacterial infection of a part of a lobe, the entire lobe, or even two lobes of one or both the lungs.
ETIOLOGY.
Following types are described:
1. Pneumococcal pneumonia. More than 90% of all lobar pneumonias are caused by Streptococcus pneumoniae, a lancet-shaped diplococcus. Out of various types, type 3-S. pneumoniae causes particularly virulent form of lobar pneumonia.
2. Staphylococcal pneumonia. Staphylococcus aureus causes pneumonia by haematogenous spread of infection.
3. Streptococcal pneumonia, β-haemolytic streptococci may rarely cause pneumonia such as in children after measles or influenza.
4. Pneumonia by gram-negative aerobic bacteria. Less common causes of lobar pneumonia are gram-negative bacteria like Haemophilus influenzae, Klebsiella pneumoniae (Friedlander's bacillus), Pseudomonas, Proteus and Escherichia coli.
MORPHOLOGY. Laennec's original description divides lobar pneumonia into 4 sequential pathologic phases:
1. STAGE OF CONGESTION: INITIAL PHASE
The initial phase represents the early acute inflammatory response to bacterial infection and lasts for 1 to 2 days.
The affected lobe is enlarged, heavy, dark red and congested. Cut surface exudes blood-stained frothy fluid.
Microscopic Examination
i) Dilatation and congestion of the capillaries in the alveolar walls.
ii) Pale eosinophilic oedema fluid in the air spaces.
iii) A few red cells and neutrophils in the intra-alveolar fluid.
iv) Numerous bacteria demonstrated in the alveolar fluid by Gram's staining.
2. RED HEPATISATION: EARLY CONSOLIDATION
This phase lasts for2 to 4 days. The term hepatisation in pneumonia refers to liver-like consistency of the affected lobe on cut section.
The affected lobe is red, firm and consolidated. The cut surface of the involved lobe is airless, red-pink, dry, granular and has liver-like consistency.
Microscopic Examination
i) The oedema fluid of the preceding stage is replaced by strands of fibrin.
ii) There is marked cellular exudate of neutrophils and extravasation of red cells.
iii) Many neutrophils show ingested bacteria.
iv) The alveolar septa are less prominent than in the first stage due to cellular exudation.
3. GREY HEPATISATION: LATE CONSOLIDATION This phase lasts for4 to 8 days.
The affected lobe Is firm and heavy. The cut surface is dry, granular and grey in appearance with liver-like consistency. The change in colour from red to grey begins at the hilum and spreads towards the periphery. Fibrinous pleurisy is prominent.
Microscopic Examination
i) The fibrin strands are dense and more numerous.
ii) The cellular exudate of neutrophils is reduced due to disintegration of many inflammatory cells. The red cells are also fewer. The macrophages begin to appear in the exudate.
iii) The cellular exudate is often separated from the septal walls by a thin clear space.
iv) The organisms are less numerous and appear as degenerated forms.
COMPLICATIONS. Since the advent of antibiotics, serious complications of lobar pneumonia are uncommon. However, they may develop in neglected cases and in patients with impaired immunologic defenses.
These are as under:
1. Organisation. In about 3% of cases, resolution of the exudate does not occur but instead it is organised. There is ingrowth of fibroblasts from the alveolar septa resulting in fibrosed, tough, airless leathery lung tissue.
2. Pleural effusion. About 5% of treated cases of lobar pneumonia develop inflammation of the pleura with effusion.
3. Empyema. Less than 1% of treated cases of lobar pneumonia develop encysted pus in the pleural cavity termed empyema.
4. Lung abscess. A rare complication of lobar pneumonia is formation of lung abscess.
5. Metastatic infection. Occasionally, infection in the lungs and pleural cavity in lobar pneumonia may extend into the pericardium and the heart causing purulent pericarditis, bacterial endocarditis and myocarditis.
CLINICAL FEATURES. The major symptoms are: shaking chills, fever, malaise with pleuritic chest pain, dyspnoea and cough with expectoration which may be mucoid, purulent or even bloody. The common physical findings are fever, tachycardia, and tachypnoea, and sometimes cyanosis if the patient is severely hypoxaemic. There is generally a marked neutrophilic leucocytosis. Blood cultures are positive in about 30% of cases. Chest radiograph may reveal consolidation.
II. Bronchopneumonia (Lobular Pneumonia)
Bronchopneumonia or lobular pneumonia is infection of the terminal bronchioles that extends into the surrounding alveoli resulting in patchy consolidation of the lung. The condition is particularly frequent at extremes of life (i.e. in infancy and old age), as a terminal event in chronic debilitating diseases and as a secondary infection following viral respiratory infections such as influenza, measles etc,
ETIOLOGY.
The common organisms responsible for bronchopneumonia are staphylococci, streptococci, pneumococci, Klebsiella pneumoniae, Haemophilus influenzae, and gram-negative bacilli like Pseudomonas and coliform bacteria.
Bronchopneumonia is identified by patchy areas of red or grey consolidation affecting one or more lobes, frequently found bilaterally and more often involving the lower zones of the lungs due to gravitation of the secretions. On cut surface, these patchy consolidated lesions are dry, granular, firm, red or grey in colour, 3 to 4 cm in diameter, slightly elevated over the surface and are often centred around a bronchiole. These patchy areas are best picked up by passing the fingertips on the cut surface.
Microscopic Examination
i) Acute bronchiolitis, ii) Suppurative exudate, consisting chiefly of neutrophils, in the peribronchiolar alveoli, iii) Thickening of the alveolar septa by congested capillaries and leucocytic infiltration, iv) Less involved alveoli contain oedema fluid.
COMPLICATIONS.
The complications of lobar pneumonia may occur in bronchopneumonia as well. However, complete resolution of bronchopneumonia is uncommon. There is generally some degree of destruction of the bronchioles resulting in foci of bronchiolar fibrosis that may eventually cause bronchiectasis.
CLINICAL FEATURES. The patients of bronchopneumonia are generally infants or elderly individuals. There may be history of preceding bed-ridden illness, chronic debility, aspiration of gastric contents or upper respiratory infection.
VIRAL AND MYCOPLASMAL PNEUMONIA (PRIMARY ATYPICAL PNEUMONIA)
Viral and mycoplasmal pneumonia is characterised by patchy inflammatory changes, largely confined to interstitial tissue of the lungs, without any alveolar exudate. Other terms used for these respiratory tract infections are interstitial pneumonitis, reflecting the interstitial location of the inflammation, andprimary atypical pneumonia, atypicality being the absence of alveolar exudate commonly present in other pneumonias. Interstitial pneumonitis may occur in all ages.
ETIOLOGY. Interstitial pneumonitis is caused by a wide variety of agents, the most common being respiratory syncytial virus (RSV). Others are Mycoplasma pneumoniae and many viruses such as influenza and parainfluenza viruses, adenoviruses, rhinoviruses, coxsackieviruses and cytomegaloviruses (CMV).
Depending upon the severity of infection, the involvement may be patchy to massive and widespread consolidation of one or both the lungs. The lungs are heavy, congested and subcrepitant. Sectioned surface of the lung exudes small amount of frothy or bloody fluid.
Microscopic Examination
I) Interstitial Inflammation: There is thickening of alveolar walls due to congestion, oedema and mononuclear inflammatory infiltrate comprised by lymphocytes, macrophages and some plasma cells. illness, chronic debility, aspiration of gastric contents or upper respiratory infection.
ii) Necrotising bronchiolitis: This is characterised by foci of necrosis of the bronchiolar epithelium, inspissated secretions in the lumina and mononuclear infiltrate in the walls and lumina.
iii) Reactive changes: The lining epithelial cells of the bronchioles and alveoli proliferate in the presence of virus and may form multinucleate giant cells and syncytia in the bronchiolar and alveolar walls.
iv) Alveolar changes: In severe cases, the alveolar lumina may contain oedema fluid, fibrin, scanty inflammatory exudate and coating of alveolar walls by pink, hyaline membrane similar to the one seen in respiratory distress syndrome.
COMPLICATIONS.
The major complication of interstitial pneumonitis is superimposed bacterial infection and its complications. Most cases of interstitial pneumonitis recover completely.
CLINICAL FEATURES.
Majority of cases of interstitial pneumonitis initially have upper respiratory symptoms with fever, headache and muscle-aches. A few days later appears dry, hacking, non-productive cough with retrosternal burning due to tracheitis and bronchitis. Chest radiograph may show patchy or diffuse consolidation.
C. OTHERTYPES OF PNEUMONIAS
I. Pneumocystis carinii Pneumonia
Pneumocystis carinii, a protozoon widespread in the environment, causes pneumonia by inhalation of the organisms as an opportunistic infection in neonates and immunosuppressed people. Almost 100% cases of AIDS develop opportunistic infection, most commonly Pneumocystis carinii pneumonia.
II. Legionella Pneumonia
Legionella pneumonia or legionnaire's disease is an epidemic illness caused by gramnegative bacilli, Legionella pneumophila that thrives in aquatic environment. It was first recognised following investigation into high mortality among those attending American Legion Convention in Philadelphia in July 1976. The epidemic occurs in summer months by spread of organisms through contaminated drinking water or in air-conditioning cooling towers. Impaired host defenses in the form of immunodeficiency, corticosteroid therapy, old age and cigarette smoking play important roles.
III. Aspiration (Inhalation) Pneumonia
Aspiration or inhalation pneumonia results from inhaling different agents into the lungs. These substances include food, gastric contents, foreign body and infected material from oral cavity. A number of factors predispose to inhalation pneumonia which include: unconsciousness, drunkenness, neurological disorders affecting swallowing, drowning, necrotic oropharyngeal tumours, in premature infants and congenital tracheo-oesophageal fistula.
1. Aspiration of small amount of sterile foreign matter such as acidic gastric contents produce chemical pneumonitis. It is characterised by haemorrhagic pulmonary oedema with presence of particles in the bronchioles.
2. Non-sterile aspirate causes widespread bronchopneumonia with multiple areas of necrosis and suppuration.
IV. Hypostatic Pneumonia
Hypostatic pneumonia is the term used for collection of oedema fluid and secretions in the dependent parts of the lungs in severely debilitated, bedridden patients. The accumulated fluid in the basal zone and posterior part of lungs gets infected by bacteria from the upper respiratory tract and sets in bacterial pneumonia.
V. Lipid Pneumonia Another variety of noninfective pneumonia is lipid pneumonia. It is of 2 types:
1. Exogenous lipid pneumonia. This is caused by aspiration of a variety of oily materials. These are: inhalation of oily nasal drops, regurgitation of oily medicines from stomach (e.g. liquid paraffin), administration of oily vitamin preparation to reluctant children or to debilitated old patients.
2. Endogenous lipid pneumonia. Endogenous origin of lipids causing pneumonic consolidation is more common. The sources of origin are tissue breakdown following obstruction to airways e.g. obstruction by bronchogenic cancer, tuberculosis and bronchiectasis.
Dental Burs: Design, Function, and Performance
Conservative DentistryDental Burs: Design, Function, and Performance
Dental burs are essential tools in operative dentistry, used for cutting,
shaping, and finishing tooth structure and restorative materials. This guide
will cover the key features of dental burs, including blade design, rake angle,
clearance angle, run-out, and performance characteristics.
1. Blade Design and Flutes
A. Blade Configuration
Blades and Flutes: Blades on a bur are uniformly
spaced, with depressed areas between them known as flutes. The design of the
blades and flutes affects the cutting efficiency and smoothness of the bur's
action.
Number of Blades:
The number of blades on a bur is always even.
Excavating Burs: Typically have 6-10 blades,
designed for efficient material removal.
Finishing Burs: Have 12-40 blades, providing a
smoother finish.
B. Cutting Efficiency
Smoother Cutting Action: A greater number of blades
results in a smoother cutting action at low speeds.
Reduced Efficiency: As the number of blades increases,
the space between subsequent blades decreases, leading to less surface area
being cut and reduced efficiency.
2. Vibration Characteristics
A. Vibration and Patient Comfort
Vibration Frequency: Vibrations over 1,300 cycles per
second are generally imperceptible to patients.
Effect of Blade Number: Fewer blades on a bur tend to
produce greater vibrations, which can affect patient comfort.
RPM and Vibration: Higher RPMs produce less amplitude
and greater frequency of vibration, contributing to a smoother experience
for the patient.
3. Rake Angle
A. Definition
Rake Angle: The angle that the face of the blade makes
with a radial line from the center of the bur to the blade.
B. Cutting Efficiency
Positive Rake Angle: Burs with a positive rake angle
are generally desired for cutting efficiency.
Rake Angle Hierarchy: The cutting efficiency is ranked
as follows:
Positive rake > Radial rake > Negative rake
Clogging: Burs with a positive rake angle may
experience clogging due to debris accumulation.
4. Clearance Angle
A. Definition
Clearance Angle: This angle provides clearance between
the working edge and the cutting edge of the bur, allowing for effective
cutting without binding.
5. Run-Out
A. Definition
Run-Out: Refers to the eccentricity or maximum
displacement of the bur head from its axis of rotation.
Acceptable Value: The average value of clinically
acceptable run-out is about 0.023 mm. Excessive run-out can lead to uneven
cutting and discomfort for the patient.
6. Load Characteristics
A. Load Applied by Dentist
Low Speed: The minimum and maximum load applied through
the bur is typically between 100 – 1500 grams.
High Speed: For high-speed burs, the load is generally
between 60 – 120 grams.
7. Diamond Stones
A. Abrasive Efficiency
Diamond Stones: These are the hardest and most
efficient abrasive stones available for removing tooth enamel. They are
particularly effective for cutting and finishing hard dental materials.
Finger Rests in Dental Instrumentation
PeriodontologyFinger Rests in Dental Instrumentation
Use of finger rests is essential for providing stability and control during
procedures. A proper finger rest allows for more precise movements and reduces
the risk of hand fatigue.
Importance of Finger Rests
Stabilization: Finger rests serve to stabilize the hand
and the instrument, providing a firm fulcrum that enhances control during
procedures.
Precision: A stable finger rest allows for more
accurate instrumentation, which is crucial for effective treatment and
patient safety.
Reduced Fatigue: By providing support, finger rests
help reduce hand and wrist fatigue, allowing the clinician to work more
comfortably for extended periods.
Types of Finger Rests
Conventional Finger Rest:
Description: The finger rest is established on the
tooth surfaces immediately adjacent to the working area.
Application: This is the most common type of finger
rest, providing direct support for the hand while working on a specific
tooth. It allows for precise movements and control during
instrumentation.
Cross Arch Finger Rest:
Description: The finger rest is established on the
tooth surfaces on the other side of the same arch.
Application: This technique is useful when working
on teeth that are not directly adjacent to the finger rest. It provides
stability while allowing access to the working area from a different
angle.
Opposite Arch Finger Rest:
Description: The finger rest is established on the
tooth surfaces of the opposite arch (e.g., using a mandibular arch
finger rest for instrumentation on the maxillary arch).
Application: This type of finger rest is
particularly beneficial when accessing the maxillary teeth from the
mandibular arch, providing a stable fulcrum while maintaining visibility
and access.
Finger on Finger Rest:
Description: The finger rest is established on the
index finger or thumb of the non-operating hand.
Application: This technique is often used in areas
where traditional finger rests are difficult to establish, such as in
the posterior regions of the mouth. It allows for flexibility and
adaptability in positioning.
MAGNESIUM
Biochemistry
MAGNESIUM
The normal serum level of Magnesium is 1.8 to 2.2. mg/dl.
Functions of Magnesium
(a) Irritability of neuromuscular tissues is lowered by Magnesium
(b) Magnesium deficiency leads to decrease in Insulin dependent uptake of glucose
(c) Magnesium supplementation improves glucose tolerance
Causes such as liver cirrhosis, protein calorie malnutrition and hypo para thyroidism leads to hypomagnesemia
The main causes of hypermagnesemia includes renal failure, hyper para thyroidism, rickets, oxalate poisoning and multiple myeloma.
Nasogastric Tube (Ryles Tube)
Oral and Maxillofacial SurgeryNasogastric Tube (Ryles Tube)
A nasogastric tube (NG tube), commonly referred to as a Ryles
tube, is a medical device used for various purposes, primarily
involving the stomach. It is a long, hollow tube made of polyvinyl chloride
(PVC) with one blunt end and multiple openings along its length. The tube is
designed to be inserted through the nostril, down the esophagus, and into the
stomach.
Description and Insertion
Structure: The NG tube has a blunt end that is inserted
into the nostril, and it features multiple openings to allow for the passage
of fluids and air. The open end of the tube is used for feeding or drainage.
Insertion Technique:
The tube is gently passed through one of the nostrils and advanced
through the nasopharynx and into the esophagus.
Care is taken to ensure that the tube follows the natural curvature
of the nasal passages and esophagus.
Once the tube is in place, its position must be confirmed before any
feeds or medications are administered.
Position Confirmation:
To check the position of the tube, air is pushed into the tube using
a syringe.
The presence of air in the stomach is confirmed by auscultation with
a stethoscope, listening for the characteristic "whoosh" sound of air
entering the stomach.
Only after confirming that the tube is correctly positioned in the
stomach should feeding or medication administration begin.
Securing the Tube: The tube is fixed to the nose using
sticking plaster or adhesive tape to prevent displacement.
Uses of Nasogastric Tube
Nutritional Support:
Enteral Feeding: The primary use of a nasogastric
tube is to provide nutritional support to patients who are unable to
take oral feeds due to various reasons, such as:
Neurological conditions (e.g., stroke, coma)
Surgical procedures affecting the gastrointestinal tract
Severe dysphagia (difficulty swallowing)
Gastric Lavage:
Postoperative Care: NG tubes can be used for
gastric lavage to flush out blood, fluids, or other contents from the
stomach after surgery. This is particularly important in cases where
there is a risk of aspiration or when the stomach needs to be emptied.
Poisoning: In cases of poisoning or overdose,
gastric lavage may be performed using an NG tube to remove toxic
substances from the stomach. This procedure should be done promptly and
under medical supervision.
Decompression:
Relieving Distension: The NG tube can also be used
to decompress the stomach in cases of bowel obstruction or ileus,
allowing for the removal of excess gas and fluid.
Medication Administration:
The tube can be used to administer medications directly into the
stomach for patients who cannot take oral medications.
Considerations and Complications
Patient Comfort: Insertion of the NG tube can be
uncomfortable for patients, and proper technique should be used to minimize
discomfort.
Complications: Potential complications include:
Nasal and esophageal irritation or injury
Misplacement of the tube into the lungs, leading to aspiration
Sinusitis or nasal ulceration with prolonged use
Gastrointestinal complications, such as gastric erosion or
ulceration