Thrombocytosis and its causes

Bones contain sponge tissue, the bone marrow, which has basic cells that are transformed into red blood cells, white blood cells, or platelets. Platelets travel through the blood vessels and suppress to clot the blood so that bleeding stops when damage to the blood vessel occurs, such as when we cut a finger.

Under normal circumstances, a platelet should have between 150.000 and 450.000 per microliter of blood and thrombocytosis a condition with an increased platelet count (over 400 x 109 / L).

If it’s caused by a bone marrow disorder, the bone marrow produces a large number of cells that make platelets and release too many platelets into the blood. If blood counts reveal a large number of platelets, it must be decided whether reactive thrombocytosis or thrombocythemia is involved.

The increased platelet count that results from the clonal disease of the pluripotent hematopoiesis stem cell, that is, the autonomic exuberance of the platelet lineage, is called primary thrombocytosis.

These include primary essential thrombocytosis or thrombocythemia and thrombocytosis in chronic myeloproliferative diseases (chronic granulocytic leukemia, polycythemia vera, osteomyelofibrosis). Primary thrombocytosis is characterized by the presence of enormous pathological megakaryocytes in the bone marrow.

Treatment consists of the administration of cytostatics, anti reactive agents and thrombocytopheresis.

Secondary or reactive thrombocytosis occurs during sideropenic anemia, chronic inflammation, malignancies, after splenectomy, after exertion, bleeding, etc. There is an increased number of megakaryocytes in the bone marrow of these patients, normal in shape and size. In addition to treating the underlying disease, it is advised to administer antiplatelet agents (acetylsalicylic acid, dipyridamole, etc.).


Reactive thrombocytosis rarely causes symptoms. Most patients do not have any symptoms at the time of diagnosis that may lead to suspected thrombocytosis. Most patients experience symptoms that result from the formation of clots in the small and medium blood vessels.

If blood platelets are too low, the risk of bleeding, including menstrual bleeding, increases. If there are too many platelets, they can cause thrombosis or blood clots – which can end in a fatal outcome. In addition, there is a reasonable risk of a heart attack or stroke.

Some of the symptoms that may occur are:



chest pain.


limb soreness when exposed to cold,

the frequent occurrence of tingling and numbness in the fingers,

temporary vision changes,

the possible onset of seizures,

weight loss,

bleeding on the skin and gums,

joint and muscle pain,

high body temperature,

enlarged liver and spleen.


Slight bleeding from the nose (epistaxis) and gums, blood in your stool, and bruising that you don’t know can sometimes occur, all of which are effective indicators of thrombocytosis. There is also a condition of over-reduced platelet concentration in the blood called thrombocytopenia. Reduced platelet concentration in the blood is considered to be any value below 150 and 450 x 109 platelets per liter of blood.

Both conditions can be life-threatening and you should see your doctor for the first symptoms to determine the diagnosis and treatment.


Treatment of reactive thrombocytosis is cause-oriented. If the cause is previous surgery or an injury that caused significant blood loss, the thrombocytosis will not last long. If the cause is a chronic infection or inflammatory disease, platelet levels may remain elevated until the condition is brought back into control.

Brain aneurysm

Brain aneurysm

A brain aneurysm is an abnormal enlargement of a blood vessel in the brain. Arteries that supply the brain are branched out from the set of arteries that is located at the base of the brain. Those branching sites are the most common locations where brain aneurysms occur. Brain aneurysms can affect anyone, including children, but the are more commonly seen in adults 35 to 60-year-old, slightly more common in women.

How does it happen?

The wall of the artery becomes weaker in some places over time and due to long-lasting pressure, an enlargement (bulge) occur. That bulge may be in the form of a sac (balloon-like) and then it is called a saccular aneurysm, which represents the most common form of this condition. The other form of brain aneurysm represents a spindle and then it‘s called a fusiform aneurysm.

As the enlargement grows, the sack expands and creates a neck that makes a connection to the artery. When the brain aneurysm is small it doesn‘t pose a greater danger, but as it grows larger it gets prone to a rupture which causes the leakage of blood into the area between the brain and the lining that separates it from the skull, called subarachnoid hemorrhage.

Signs and symptoms

In some cases, people with an aneurysm do not have any symptoms at all. Because the growth of the aneurysm can pressure the surrounding tissue, symptoms such as headache, diplopia (double images), lower eyelid, pain behind or above the eye, trigeminal neuralgia, or uneven pupils may occur.

Symptoms of aneurysm rupture: sudden, extremely (as never before) severe headache, nausea, vomiting, neck stiffness, changes in consciousness to coma.

Massive intraventricular hemorrhage usually gives a very difficult clinical picture: deep coma, hyperpyrexia, decerebrate rigidity. It almost always ends in death.


Brain aneurysm rupture

The rupture of brain aneurysms involves the breaking of blood vessels in the brain. This leads to hemorrhage in the area of the brain membranes, sometimes leading to hematoma or penetration of blood into the ventricular system. All of this together causes brain damage. In 40 percent of cases of a brain aneurysm that suddenly cracks can be the cause of death, and if the patient survives, each new rupture in the next 15 days increases the mortality rate by up to 70 percent.

Risk factors for brain aneurysm rupture

The most common risk factors for brain aneurysm rupture are hypertension, smoking, patient age (ruptures are more common after 40 years), atherosclerosis, use of medications such as aspirin or anticoagulant therapy, cocaine use, alcohol consumption, head injury, and low doses of estrogen after menopause. Brain aneurysms are more common in women after menopause. A family history of aneurysms is another risk. It should also be noted that certain diseases, such as polycystic disease and AV brain malformations, formerly associated with aneurysms.

Brain aneurysm rupture vs stroke

The concepts of brain aneurysm rupture and stroke should be separated. In the case of a rupture, bleeding occurs in the brain, which gives a clinical picture of a sudden headache, unlike a stroke, where the clinical picture is followed by a sudden resulting half-body paralysis and loss of speech. However, after a rupture, there may be a stroke as a result of the blood vessel spasm. The classic cause of brain infarction is the closure of a blood vessel by a thrombus, most often scattered from the heart during arrhythmia, or stenosis of the blood vessels of the neck and brain.

brain aneurysm


In cases of aneurysm rupture or significant enlargement, treatment is always surgical. Before surgery, it is necessary to determine the condition of the cardiovascular system of the patient, since atherosclerosis is also present in a large number of patients.

Whether it is an aneurysm rupture or not, therapy is surgical, in the domain of a neurosurgery specialist.

Surgical clipping on the neck of the aneurysm involves a neurosurgical procedure in which a thin metal clip is placed in a place of the neck of the aneurysm, which presses the neck of the sacral aneurysm and prevents blood supply to it.

Endovascular coiling is a procedure similar to angiography when an aneurysm catheter is placed and a small metal coil or balloon is placed in it to stop the blood flow to the aneurysm.

In cases where a person is found to have a small, asymptomatic aneurysm, depending on the size, location, growth of the aneurysm, and on the age of the patient, it depends on whether one of these methods is immediately followed, or whether the patient will be monitored.



Thrombocytopenia represents a decrease in the number of blood cells called blood platelets, which may cause bleeding in the skin and internal organs. This is a lack of blood platelets, small blood cells that play a key role in the closure of damaged blood vessels may cause excessive bleeding. Normal blood platelet count in blood is 150 – 450 x 109/L.

Signs and symptoms

An enlarged spleen that can be determined by clinical examination – palpation or ultrasound is one of the possible signs and symptoms. Detection of an enlarged liver can also point out to possible chronic liver disease, which may be another cause of thrombocytopenia.

Skin bleeding appears most often in the form of small red spots that do not vanish after exposed to pressure – petechiae when the platelet count gets significantly reduced. They are most often located in the area of the ankles and feet. Furthermore, bleeding in the gums and in the oral cavity may occur.

The skin bleeding, larger of petechiae. called purpura, or ecchymosis, a skin bleeding similar to a hematoma, which is most often located on the feet, but also in other parts of the body may occur. Ultimately, stool bleeding, urinary tract infections or prolonged menstrual bleeding can lead to a significantly lower number of platelets.


Thrombocytopenia may be hereditary or caused by various different reasons. Some of the important ones include:

Decreased production of platelets – Thrombocytopenia due to decreased production of platelets is most commonly occurring with the decreased production of other blood cells, such as in leukemia or myelodysplastic syndrome. Another possible cause may be the absence of vitamin B12 or folic acid, viral and bacterial infections, sepsis, and liver failure.

breaking down

Increased breakdown of platelets – A number of various conditions such as pregnancy, hemolytic uremic syndrome, autoimmune diseases, certain medications, thrombotic thrombocytopenic purpura may cause an increased breakdown of platelets, so when platelets are getting destroyed faster than they are produced that results in reduced blood platelet count.

Platelets trapped in the spleen – A disorder of redistribution of platelets in circulation occurs when the spleen is enlarged. Normally, there are about 30% platelets in the spleen and an enlarged spleen stores up to 90%, while there are few in the circulation. The platelet life is normal and there is no increased risk of bleeding. If the enlarged spleen is associated with liver cirrhosis, blood coagulation is disturbed and there is a risk of bleeding.


Thrombocytopenia treatment depends on the cause and severity of the condition. The main goal of the treatment is to achieve a sufficient number of platelets, preventing serious bleeding.

Mild thrombocytopenia sometimes does not need to be treated because bleeding can stop normally. In severe thrombocytopenia, on the other hand, the doctor will prescribe medication to you or change the drugs you are currently taking to stop their side effects.

transfusion in Thrombocytopenia treatment

Treatment of the underlying cause of thrombocytopenia when your doctor identifies a condition that is causing thrombocytopenia will improve the signs and symptoms.

Drugs and therapeutic procedures used to stabilize serious conditions caused by thrombocytopenia may include blood or platelet transfusion, splenectomy (surgical removal of the spleen), plasma exchange, or use of corticosteroids or immunoglobulins, which block the effects of the immune system.

Epistaxis (Nosebleed)

Epistaxis – epidemiology

Epistaxis represents bleeding from a nose, and it is fairly common phenomena which can occur at any age, but it is most common in young children (2 – 10 years) and elderly population as opposed to older children and adults. Moreover, epistaxis is very rare in very young children (< 2 years) where it is often caused by serious illness or trauma. Approximately more than 50% of all people will experience epistaxis at some point in their life. A nosebleed can be quite dramatic and abundant, but it is rarely life-threatening or deadly because around 10% of these nosebleeds are seen as serious conditions.

Classification and causes of epistaxis

Nosebleeds can be induced by various causes, and depending on them epistaxis can be divided into two categories – Anterior bleeding (frontal and the most common bleeding) and Posterior bleeding (less common, but more serious, back bleeding). Some of the main causes of both epistaxis types are listed below.

Anterior epistaxis causes

nose-picking – especially if it’s done with nails, and aggressively

nasal congestion – a blockage of the nasal passages, often due to cold or flu

nose lesion – small wound inside the nose

foreign body – epistaxis can occur after the elimination of the foreign body from the nose

nose-blowing – if it’s done aggressively

anatomical disorders – deviation of the nasal septum (the wall between the left and right nostrils) or sensitive nasal blood vessels

dry air – dry air or high temperatures that can affect the nasal mucous membrane

sinusitis – inflammation of the cavities around the nasal passage

allergic / nonallergic rhinitis – irritation or inflammation of nasal mucous membrane caused by allergens or other agents

overuse of nasal decongestants – rebound phenomenon of nasal sprays can cause a epistaxis

Epistaxis (nosebleed)

Posterior epistaxis causes

severe nasal injuries – such as a nasal fracture (broken nose) or surgeries done on the nose

anticoagulants (blood thinners) – drugs used to prevent blood clotting (coagulation) whose main side effect is bleeding as they decrease the blood clotting ability

antiplatelet drugsdrugs used to prevent arterial thrombosis, by inhibiting the platelet plug formation, which may induce bleeding

thrombolyticsclot-busting agents that may also lead to bleeding

coagulopathy – a disorder in a blood clotting ability such as Von Willebrand’s disease or hemophilia

malignant or benign tumor – in thenasal cavity

atherosclerosis – narrowing of the artery caused by a plaque

hypertensionalthough it is not a direct cause of epistaxis, people with high blood pressure can experience heavy nosebleeds that can be hard to stop

Signs and symptoms

The signs and symptoms of the people with epistaxis depend on bleeding intensity. A person will have visible signs of bleeding from the nose which can sometimes pass to the mouth. If the bleeding is severe, prominent paleness can be observed as well as accelerated pulse. The individual can be upset which can sometimes seem like a panic because of the dramatic effect caused by sudden bleeding.

First aid

A patient with epistaxis can take some steps that will ease the bleeding or stop it before coming to the doctor. One of the most important things to do is to stay focused and not panic. It is necessary to wash your face with cold water, pressing the soft part of your nose firmly for about 10 – 15minutes. Sitting upright while leaning your head forward can reduce the blood pressure in the nasal blood vessels. Moreover, it is advised to place an ice pack in a towel on the bridge of the nose to narrow the blood vessels. Don’t bend your head backward because blood from the nose will pass through your throat and you will swallow it. If the bleeding is serious and lasts long, and/or you have trouble breathing, call a doctor immediately.

Platelets (Thrombocytes)

Platelets (Thrombocytes) represent the fragments of the cell named megakaryocyte, which is a type of bone marrow cells sent into the circulation. Thrombocytes are small and oval plates with a diameter of only 2 – 4 mm. Normal platelet count range from 150.000 – 450.000 per μL of blood.

Platelet development

Megakaryocyte comes from hematopoietic stem cell precursors from the bone marrow like all other blood cells. Its transformation into a defined stem is the beginning of the thrombocytopoiesis process. Megakaryoblast is formed from the myeloid stem cell after which it becomes a megakaryocyte. Due to its large size, a megakaryocyte can‘t leave the bone marrow, but it adheres to the walls of the sinus capillary, partially participating in the formation of its wall. As the cell consists of segments, its parts are separated and put into circulation as platelets. Several thousand platelets can be made from one megakaryocyte. Thrombocytes do not come from the normal cell division, as they have no core, and in the true sense of the word, they are not cells. Therefore, the more adequate name is platelet. However, the name thrombocyte is still used sometimes.


Platelet maturation is regulated by factors of colony growth that controls the production of megakaryocytes. In addition to that, a plasma protein which facilitates the maturation of megakaryocytes and their fragmentation called thrombopoietin is constantly being generated in the liver and kidneys.

Structure of platelets


Platelets have a very complex structure. Their membrane consists of three layers including

The outer shell – which is responsible for platelet adhesion and aggregation

Middle layer – which represents a source of platelet phospholipids involved in the blood clotting process

The inner layer – which is responsible for the platelet shape


Platelet cytoplasm also has a very complex structure. It contains an open channel system responsible for the discharge of the platelet granules’ content into the outer environment. Moreover, the cytoplasm contains a powerful contractile system that allows an easy change in the platelet‘s shape.

Role in the organism

The main role of platelets is in hemostasis, a process of bleeding stopping in an injured blood vessel. Hemostasis is a process that reduces or prevents blood loss in times of blood vessel injuries. As the blood in the blood vessels is under pressure, cutting or spraying the blood vessel results in blood leakage, and this phenomenon is called bleeding (hemorrhage). If a small blood vessel is injured, bleeding is usually spontaneously stopped by the hemostasis process. However, in the case of injuries of large arteries and veins, hemostasis is not as effective and the injuries must be surgically sanitized. After the damage to the wall of the blood vessel, blood clots accumulate at the site of the injury where they

1. Liberate the substances that cause the blood vessel to contract, which reduces the blood loss

2. Form an aggregate, a platelet plug at the site of the injury

3. Participate in the process of blood clotting, due to coagulation factors that contain

4. Take part in the healing of the injury.



Platelets begin to adhere to collagen fibers within a few seconds after the occurrence of the damage to the inner part of a blood vessel, and that process is called platelet adhesion. Adhered platelets are activated and they alter their shape while emptying their granules that stimulate further aggregation. The interconnection of a large number of platelets at the site of a blood vessel injury is called platelet aggregation.

Platelet life span

Circulating platelets have a lifespan of 1 to 2 weeks. Older blood platelets, which are not used during blood clotting, are destroyed by macrophages from liver and spleen. A spleen is not just a place which destroys old platelets, as it is also an important reservoir of these blood elements. It releases a large number of stored platelets into the circulation under the influence of the nervous system in certain occurrences including bleeding or burns.


An increased platelet count called thrombocytosis increases the tendency of a pathological blood clot (thrombus) formation. That blood clot can induce life-threatening complications such as heart attack and ischemic stroke. A decrease in blood platelet count is called thrombocytopenia. Physiological thrombocytopenia occurs normally in the women immediately prior to menstrual bleeding. Female sex hormones reduce the formation and maturation of blood platelets. Severe thrombocytopenia causes spontaneous bleeding, especially in the gums and digestive tract.