Browsed by
Category: Pathology




INTRODUCTION: It is an important element to have a detailed view of the procedure known as Lumbar puncture which is also known as the Spinal Tap.

It is mostly used as a diagnostic procedure by which a sample of CSF can be obtained, (which is known as the Cerebrospinal Fluid, the fluid found in the brain and spinal cord.) which is used for bacterial or microscopic examination in the case of meningitis, as well as providing a way for injecting drugs like in the case of chemotherapy. Anesthetic drugs and antibiotics are also injected into the Cerebrospinal fluid via the Spinal tap. This procedure also provides a means of measuring the pressure in the Cerebrospinal fluid with the help of a manometer.

Cerebrospinal Fluid is a clear colorless fluid produced by the choroid plexus and assisted by the ependymal cells. It contains inorganic salts like chloride, glucose few lymphocyte cells and trace amounts of protein. The pressure range of cerebrospinal fluid measured by the manometer is said to be about 60 – 150mm water and the rate of the production of cerebrospinal fluid is 0.5ml/min. (Snells Neuroanatomy)

The basic function of cerebrospinal fluid is to cushion or protect the brain from any mechanical trauma. It also provides buoyancy to the brain due to the increased density of the cerebrospinal fluid. The fluid also acts as a source of nourishment for the underlying nervous tissue and also acts as a pathway for the pineal secretions from the pituitary gland.

Method: The patient, on whom the lumbar puncture is to be performed should lie in a lateral Recumbent position i.e. on the side or even in a prone or sitting position depending on the preference of the health caregiver or a clinician. The vertebral column should be well flexed and the lamina in the lumbar region should be opened to the maximum.

There is an imaginary line which is obtained by joining the highest points on the iliac crests and when joined passes over the fourth lumbar vertebrae. From L3 to the lower border of the S2 vertebrae the subarachnoid space filled with cerebrospinal fluid is accessible and safe to penetrate as the spinal cord in an adult already terminates at the level of L1 and L2 vertebrae, thus making the lumbar region an ideal site to perform the Spinal tap.

The physician then uses a careful aseptic technique and the patient is provided with local anesthesia. The lumbar puncture needle that is the Quincke spinal needles 22G which may be of size 1.5 for infants and newborn, 2.5 for children and 3.5 for adults, fitted with a stylet is passed through anatomical structures like the skin, superficial fascia, Supraspinous ligament, Interspinous ligament, Ligamentum flavum, areolar tissue (which contains the internal vertebral venous plexus), Dura mater and the Arachnoid mater, ending in the subarachnoid space which contains the cerebrospinal fluid. It is from here that we are able to aspirate a sample of cerebrospinal fluid. The needle will pass through these structures to a depth of 1inch (2.5cm) in a normal adult and less in a child, however, in the case of an obese patient a depth of 4 inches is required.

When the stylet is withdrawn and if few drops of blood are seen, it is then due to the fact that the needle has only entered the internal vertebral plexus and might still be in the areolar tissue. The patient would experience a fleeting discomfort in a muscle or a dermatome if the nerve roots of the cauda equina were stimulated. If the needle is in the lumbar cistern and the stylet is withdrawn the cerebrospinal fluid would start flowing and escapes at a rate of approximately one drop per second. The cerebrospinal fluid’s normal pressure is about to 60 -150mm of water and if the subarachnoid pressure is high then the fluid would escape out as a jet.

Anesthetic drugs are also given in the extradural space and in the subarachnoid space in order to anesthetize the nerve roots of the lumbar and sacral area, which is helpful in operations of the pelvic and the leg. The patient is advised to be in an erect position during these surgeries as if the patient is in a recumbent position then the anesthesia would be only effective unilaterally and if the patient is in a head-down position the anesthetic could pass cranially and affect respiration.

Some of the complications include Post-dural puncture headache, infection, cerebral herniation, bleeding and back pain. It is contraindicated when there is an increased intracranial pressure, thrombocytopenia or any brain abscess.

Types of equipment used:

Sterile gloves

1% lidocaine solution

22G or 25G needle

5ml disposable syringe

Sterile drape

Spinal needle with stylet

Manometer with 3 way stopcock

A labeled sterile specimen container

Sterile bandage

You must know these things about Embolism

You must know these things about Embolism


  • An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or infarction.
  • The vast majority of emboli are dislodged thrombi, hence the term thromboembolism.
  • Other rare emboli are composed of fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or even foreign bodies.
  • Emboli travel through the blood until they encounter vessels too small to permit further passage, causing partial or complete vascular occlusion.

C:\Users\user\AppData\Local\Microsoft\Windows\Temporary Internet Files\Content.Word\Embolism.jpg


Types of Emboli

Some important types of embolism

  • Pulmonary Embolism:
  1. Pulmonary emboli originate from deep venous thromboses and are the most common form of thromboembolic disease.
  2. Incidence since the 1970s of roughly 2 to 4 per 1000 hospitalized patients in the United States.
  3. PE causes about 100,000 deaths per year in the United States.
  4. In more than 95% of cases, PEs originates from leg DVT.
  5. Course of embolus causing Pulmonary Embolism

  1. Rarely, a venous embolus passes through an interatrial or interventricular defect and gains access to the systemic arterial circulation (paradoxical embolism).
  2. Most pulmonary emboli (60% to 80%) are clinically silent because they are small. With time they become organized and are incorporated into the vascular wall; in some cases organization of the thromboembolus leaves behind a delicate, ridging fibrous web.
  3. Sudden death, right heart failure (cor pulmonale), or cardiovascular collapse occurs when emboli obstruct 60% or more of the pulmonary circulation.
  4. Embolic obstruction of medium-sized arteries with subsequent vascular rupture can result in pulmonary hemorrhage but usually does not cause pulmonary infarction. This is because the lung is supplied by both the pulmonary arteries and the bronchial arteries, and the intact bronchial circulation is usually sufficient to perfuse the affected area. Understandably, if the bronchial arterial flow is compromised (e.g., by left-sided cardiac failure), infarction may occur.
  5. Embolic obstruction of small end-arteriolar pulmonary branches often does produce hemorrhage or infarction.
  6. Multiple emboli over time may cause pulmonary hypertension and right ventricular failure.

Figure- Embolus from a lower extremity deep venous thrombosis,

lodged at a pulmonary artery branchpoint.

Systemic Thromboembolism

  1. Most systemic emboli (80%) arise from intracardiac mural thrombi, two thirds of which are associated with left ventricular wall infarcts and another one fourth withleft atrial dilation and fibrillation. The remainder originates from aortic aneurysms, atherosclerotic plaques, valvular vegetations, or venous thrombi (paradoxical emboli);10% to 15% are of unknown origin.
  2. Arterial emboli are in contrast to venous emboli, the vast majority of which lodge in the lung, arterial emboli can travel to a wide variety of sites; the point of arrest depends on the source and the relative amount of blood flow that downstream tissues receive.
  3. The emboli are arterial and invariably cause infarction at the sites of lodgement . These sites, in descending order of frequency are: lower extremities (75%) or the brain (10%), internal visceral organs; the intestines, kidneys, spleen, and upper extremities, may be involved on occasion.
  4. The consequences of systemic emboli depend on the vulnerability of the affected tissues to ischemia, the caliber of the occluded vessel, and whether a collateral blood supply exists; in general, however, the outcome is tissue infarction.

C:\Users\user\AppData\Local\Microsoft\Windows\Temporary Internet Files\Content.Word\pic-heart-attack.jpg

Fat and Marrow Embolism

  1. Microscopic fat globules—sometimes with associated hematopoietic bone marrow—can be found in the pulmonary vasculature after fractures of long bones or, rarely, in the setting of soft tissue trauma and burns. Presumably these injuries rupture vascular sinusoids in the marrow or small venules, allowing marrow or adipose tissue to herniated into the vascular space and travel to the lung.
  2. Fat and marrow emboli are very common incidental findings after vigorous cardiopulmonary resuscitation and are probably of no clinical consequence. Indeed, fat embolism occursin some 90% of individuals with severe skeletal injuries but less than 10% of such patients have any clinical findings.
  3. Fat embolism syndrome is the term applied to the minority of patients who become symptomatic. It is characterized by pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia, and is fatal in about 5% to 15% of cases. Typically, 1 to 3 days after injury there is a sudden onset of tachypnea, dyspnea, and tachycardia; irritability and restlessness can progress to delirium or coma.
  4. Thrombocytopenia is attributed to platelet adhesion to fat globules and subsequent aggregation or splenic sequestration; anemia can result from similar red cell aggregation and/or hemolysis.
  5. A diffuse petechial rash (seen in 20% to 50% of cases) is related to rapid onset of thrombocytopenia and can be a useful diagnostic feature.
  6. Fat microemboli and associated red cell and platelet aggregates can occlude the pulmonary and cerebral microvasculature.
  7. Release of free fatty acids from the fat globules exacerbates the situation by causing local toxic injury to endothelium, and platelet activation and granulocyte recruitment (with free radical, protease, and eicosanoid release) complete the vascular assault. Because lipids are dissolved out of tissue preparations by the solvents routinely used in paraffin embedding, the microscopic demonstration of fat microglobules typically requires specialized techniques, including frozen sections and stains for fat.

Figure– Bone marrow embolus in the pulmonary circulation. The cellular elements on the left side of the embolus are hematopoietic cells, while the cleared vacuoles represent marrow fat. The relatively uniform red area on theright of the embolus is an early organizing thrombus.

Air Embolism

  1. Gas bubbles within the circulation can coalesce to form frothy masses that obstruct vascular flow and cause distal ischemic injury.
  2. For example, a very small volume of air trapped in a coronary artery during bypass surgery, or introduced into the cerebral circulation by neurosurgery in the “sitting position,” can occlude flow with dire consequences.
  3. A particular form of gas embolism, called decompression sickness, occurs when individuals experience sudden decreases in atmospheric pressure.
  4. Scuba and deep sea divers, underwater construction workers, and individuals in unpressurized aircraft in rapid ascent are all at risk. When air is breathed at high pressure (e.g., during a deep sea dive), increased amounts of gas (particularly nitrogen) are dissolved in the blood and tissues. If the diver then ascends (depressurizes) too rapidly, the nitrogen comes out of solution in the tissues and the blood.
  5. The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints is responsible for the painful condition called the bends
  6. In the lungs, gas bubbles in the vasculature cause edema, hemorrhage, and focal atelectasis or emphysema, leading to a form of respiratory distress called the chokes. A more chronic form of decompression sickness is called caisson disease (named for the pressurized vessels used in bridge construction; workers in these vessels suffered both acute and chronic forms of decompression sickness).
  7. In caisson disease, persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis; the more common sites are the femoral heads, tibia, and humeri. Individuals affected by acute decompression sickness are treated by being placed in a chamber under sufficiently high pressure to force the gas bubbles back into solution. Subsequent slow decompression permits gradual resorption and exhalation of the gases, which prevents the

obstructive bubbles from reforming.

Amniotic Fluid Embolism

  1. Amniotic fluid embolism is the fifth most common cause of maternal mortality worldwide; it accounts for roughly 10% of maternal deaths in the United States and results in permanent neurologic deficit in as many as 85% of survivors.
  2. Amniotic fluid embolism is an ominous complication of labor and the immediate postpartum period.
  3. Although the incidence is only approximately 1 in 40,000 deliveries, the mortality rate is up to 80%. The onset is characterized by sudden severe dyspnea, cyanosis, and shock, followed by neurologic impairment ranging from headache to seizures and coma.
  4. If the patient survives the initial crisis, pulmonary edema typically develops, frequently accompanied by disseminated intravascular coagulation.
  5. The underlying cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins.
  6. Classicfindings at autopsy include the presence of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tract in the maternal pulmonary microvasculature
  7. Other findings include marked pulmonary edema, diffuse alveolar damage and the presence of fibrin thrombi in many vascular beds due to disseminated intravascular coagulation.

C:\Users\user\AppData\Local\Microsoft\Windows\Temporary Internet Files\Content.Word\I9EREGj.jpg

Figure-Amniotic fluid embolism. Two small pulmonary arterioles are packed with laminated swirls of fetal squamous cells. There is marked edema and congestion. Elsewhere the lung contained small organizing thrombi consistent with disseminated intravascular coagulation. (Courtesy Dr. Beth Schwartz, Baltimore, Md.)

C:\Users\user\AppData\Local\Microsoft\Windows\Temporary Internet Files\Content.Word\wInmkkS.JPG

Skip to toolbar