Priapism is the negative side of prolonged erection. What is priapism in men

When the penis is erected, arterial blood flow increases and smooth muscles relax. Violation of the outflow of venous blood from the penis causes a persistent painful erection.

Priapism causes quite a bit of discomfort

This painful condition is called priapism. The pathology is rare and has nothing to do with sexual arousal. Prolonged involuntary erection differs from real arousal in that the head of the penis remains relaxed when the corpora cavernosa are filled.

The disease can occur not only in adult men, but also in boys.

Causes of the disease

Priapism develops at any age and can be either a primary disease or a complication of injury or disease. The main cause of the disease is impaired blood flow: increased flow of arterial blood to the corpora cavernosa and stagnation of venous blood.

Priapism can also occur as a result of taking drugs to enhance potency. The use of antidepressants, psychotropic drugs, indirect coagulants, drugs to lower blood pressure also cause priapism.

When treating impotence, medications can be injected into the cavernous bodies and urethra, which subsequently lead to disruption of blood flow in them.

Priapism can be a secondary disease as a consequence of blood diseases, tumors and injuries of the spinal cord and brain, diseases of the male genital organs, diabetes mellitus, renal failure, thrombosis.

Alcoholism and drug addiction can also cause the disease. Priapism is often caused by mental illness, stress, and allergies. In boys, priapism can be caused by blood diseases.

Symptoms

Priapism usually occurs suddenly, most often at night, and is accompanied by severe tension of the penis. Attacks at night are accompanied by short-term tension. Over time, erections become more frequent and painful. After waking up or having a bowel movement bladder, the tension in the penis weakens.

True priapism also begins suddenly, but unlike nighttime priapism, it continues after waking up. The intensity of pain during an attack depends on the filling of the cavernous bodies.

The pain is localized at the root of the penis and radiates to the perineum. Sometimes swelling occurs after an attack. The duration of the attack can be from several hours to several months.

Priapism is accompanied by attacks of pain that can last for months

Penile tension is not associated with arousal. Sexual intercourse does not end with ejaculation and does not bring satisfaction, but only intensifies the painful sensations. Pain makes it difficult to urinate and defecate.

The disease is characterized by a peculiar erection. The penis tenses in an arched manner. The head of the penis is not tense and is turned towards the abdomen.

Classification

The following types of priapism are distinguished:

• ischemic;
• not ischemic.

Ischemic priapism

With vascular imbalance, the outflow of venous blood occurs. Oxygen starvation (ischemia) increases in the tissues of the penis. At long-term stress Destructive changes begin in the cells. If an attack lasts more than three days, irreversible processes in tissues may occur.

Due to insufficient blood supply, the head of the penis turns black, and the penis itself becomes bluish in color. The attacks are accompanied by acute pain. Prolonged ischemia of the penis leads to necrosis or gangrene.

Not ischemic priapism

The development of priapism not associated with ischemia is associated with injury. The disease can also occur due to abnormalities vascular system. When an injury occurs, the penis becomes filled with blood, which is slowly removed through the veins. As a result, tension in the penis occurs, which does not go away after intercourse. An attack of non-ischemic priapism is accompanied by dull pain.

Consequences

The consequences of priapism depend on its type. Priapism associated with ischemia can cause necrosis of penile tissue. Severe cases of attacks can result in gangrene and amputation of the penis.

Severe forms of priapism can lead to very disastrous consequences

Complications of non-ischemic priapism are not as dangerous, but still pose serious problems. When blood circulation is impaired, inflammation of the corpora cavernosa occurs. The head of the penis remains undamaged. Both types of priapism can cause sexual dysfunction.

Diagnostics

Diagnosis of the disease includes examination of the patient, X-ray and ultrasound examination, duplex scanning of blood vessels, as well as puncture of the corpora cavernosa. Palpation reveals tension in the penis.

Duplex scanning makes it possible to make a differential diagnosis of priapism, identify its types and vascular anomalies. Puncture of the corpora cavernosa allows one to identify the type of disease. Ischemic priapism is characterized by dark-colored blood.

Treatment

The effectiveness of treatment depends on diagnosing priapism in the early stages. Treatment of priapism can be conservative or surgical. At conservative method prescribe:

• cooling the penis (use an ice pack);
• administration of drugs that stop an attack of priapism.

If conservative treatment of priapism does not produce results and relapses of the disease occur, surgical intervention is performed, during which the outflow of blood from the cavernous bodies is restored. The most effective are spogiocavernous or safengocavernous anastomosis.

X-ray contrast cavernosography is also performed, in which blood is aspirated from the cavernous bodies and washed with anticoagulants.

With the death of the cavernous bodies, the only way restoration of erection - implantation of prostheses. In case of necrotic lesions and gangrene of the penis, amputation is indicated.

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The disease priapism received its name from the ancient god of fertility, debauchery and voluptuousness, Priapus, who is represented in all images and sculptures with an erect phallus.

Unfortunately, this illness is not a “divine pleasure.” It is a serious pathology with a prolonged, painful erection that is not associated with sexual arousal and does not end after ejaculation. The erectile state can last for several hours.

What priapism is, a small number of men know from their own experience - 0.11-0.4% of the number suffering from various kinds of urological ailments. However, this disease deserves attention due to the fact that its consequences can be very serious.

The development of priapism can occur at any age, but most often it occurs in boys before puberty and in men during active sexual activity.

The main cause of involuntary painful erection is disruption of blood flow in the cavernous (cavernous) bodies of the penis. If a significant influx of arterial blood leads to overflow of the corpora cavernosa, usually due to trauma, non-ischemic priapism occurs. In cases where the venous outflow from the penis worsens, the blood stagnates and its properties change, veno-occlusive or ischemic priapism occurs.

The etiology of ischemic priapism is varied.

1. Direct injection of vasoactive drugs into the cavernous tissue during treatment. The risk of an attack is especially high when using papaverine.
2. Hematological diseases. With increased blood viscosity, adhesion of blood elements and thrombus formation occurs. In 23% of men and 63% of children, ischemic priapism occurs against the background of sickle cell anemia. In 1% of all cases, the cause is leukemia.
3. Cancers (prostate, bladder, kidney, colon, genitourinary system) and accompanying metastatic processes into the cavernous tissue or venous collectors of the pelvis block venous outflow from the penis.
4. Taking psychotropic, narcotic, antihypertensive drugs, alcohol, antidepressants.
5. In 12%, perineal trauma leads to ischemic priapism. When tissue swells at the base of the penis, thrombosis occurs.
6. Diseases and injuries of the central nervous system, such as tumors, multiple sclerosis, brain injuries (brain and spinal cord).
7. Psychoneurological factors.

If the cause of involuntary erection is not clear, and this happens in 30-60% of patients, priapism is given the name idiopathic.

Etiology of non-ischemic arterial priapism

Blunt trauma to the penis or perineum is almost always the cause of arterial priapism - rupture of the cavernous artery or its branches. After vascular surgery to restore erectile dysfunction, this condition is less common. There are cases that arterial priapism manifests itself several days after injury. This is explained by the fact that a blood clot formed in the damaged artery resolves after some time.

It is believed that an arterial form of the disease may exist long time without consequences for the cavernous bodies. In medical practice, there have been cases when this form of priapism was observed in patients for several years while maintaining potency.

Intermittent nocturnal priapism is the episodic occurrence of ischemic priapism, usually during sleep. In this case, each episode either goes away on its own or is successfully treated with aspiration of the cavernous bodies or intracavernous injections of adrenergic agonists. Nocturnal priapism is characterized by maximally tense penis. Erections are short-term, but painful. After waking up, defecating, and active movements, the erection weakens.

Nocturnal priapism can occur at any age. At first, awakenings in the middle of the night due to an erection occur occasionally (once a week or 10 days); over time, they occur every night and more than once.

The etiology of intermittent priapism is poorly understood, but it is believed that it arises from a defect in smooth muscle with an increased tendency to relax.

Treatment of this condition involves systemic prophylactic treatment to prevent future attacks of priapism episodes, including self-administration of an intracavernosal adrenergic agonist injection, antiandrogen therapy, acupuncture and, as a final treatment option, penile replacement.
Also, when a diagnosis of “nocturnal priapism” is made, long-term therapy with antidepressants and tranquilizers is prescribed, and it is recommended to consult a psychotherapist.

Common Causes of Priapism

Priapism may occur due to the following medications:

• drugs that enhance erectile function - Viagra, Levitra, etc.;
• antidepressants and sedatives - Buporpion, Prozac, Valium, Diazepam;
• indirect anticoagulants - Heparin, Warfarin;
• psychotropic drugs - Zyprexa, Risperidone;
• drugs injected into the penis to treat impotence.

In addition, prolonged involuntary erection of the penis is a consequence of certain diseases:

• anemia, leukemia;
• brain tumors;
• spinal cord injuries;
• diseases of the genitourinary system (tumors, injuries, etc.);
• metabolic disorders (diabetes mellitus);
• intoxication (alcohol, drugs).

Symptoms

As a rule, the urinary process is not disturbed, since in this case the overflow of blood occurs in the cavernous bodies, and the head, prostate and urethra do not participate in the erection. The head of the penis is flabby and small, the surface of the penis is smooth without any bulges caused by the erection of the corpus spongiosum located around the urethra.

With ischemic priapism, there are severe pain in the penis and perineum several hours after the attack. Swelling of the penis may occur and foreskin. During sexual intercourse there is no relief, and sometimes the pain only intensifies. With arterial ischemic priapism, the patient usually does not experience pain, since the venous outflow is normal.

The absence or presence of pain makes it possible to distinguish the ischemic form from the non-ischemic one.

The type of priapism is determined using a blood gas test. A thin needle is used to draw blood from the penis. If the blood is dark, it is most likely a case of ischemic priapism; if it is light red, it is most likely non-ischemic. More accurate test results are obtained through laboratory tests.

In most cases, an ischemic type of priapism is observed, when the oxygen level in the blood entering the cavernous bodies decreases, pain appears and damage to the smooth cavernous muscles develops. If left untreated, there is a risk of developing cavernous fibrosis, which can lead to loss of normal erection.

If an erection lasts more than 4 hours, a man should seek help from a urologist. But, unfortunately, the patient, due to false shame, turns to the doctor a day later or later.

Prolonged priapism dramatically increases the incidence of erectile dysfunction. Taking into account the peculiarities of the course of the disease, treatment of priapism should be fast, effective and step-by-step, aimed at maintaining potency.

Ischemic priapism treatment:

If the patient consults a doctor within 6 hours of the onset of the attack, he is prescribed a cold compress, intravenous or intramuscular injections of Relanium, and drugs that improve blood properties.

In case of an attack lasting more than 6 hours, the following is carried out:

• aspiration of blood and irrigation of the cavernous bodies (efficiency 30%);
• intracavernous administration of adrenergic drugs (efficacy 58%)
• sequential aspiration/irrigation with intracavernous injections.

The use of any sympathomimetic agent can stop an attack of priapism, however, when using adrenaline, tachycardia and arrhythmia occur, and when using metaraminol there is a risk of developing a severe form of hypertension. Minimum quantity side effects are caused by the use of phenylephrine, mezatone.

Treatment of priapism (ischemic), which lasts more than 24 hours, with adrenergic agonists should be carried out with great caution, as this can lead to increased ischemia of the cavernous tissue.

If the attack lasts more than 48 hours, there is a need for shunt surgery or endophalloprosthetics, since during this period the functionality of the smooth muscles is impaired. The effectiveness of adrenergic drugs is practically absent.

Shunt operations are aimed at improving venous outflow from the cavernous bodies.

Priapism that occurs against the background of a hematological factor has some features. The patient is given intravenous alkaline solutions, a reduction in blood levels is carried out using the hypertransfusion method. pathological hemoglobin S, rehydration, plasmapheresis, etc. are performed. After this, treatment of priapism occurs according to standard methods (aspiration/irrigation of the cavernous bodies, intracavernous injections of adrenomimetic drugs).

In case of irreversible changes, when the outcome is cavernous fibrosis, penile prosthesis is the only method of restoring normal physiological potency.

Endofalloprosthetics is excluded in the following cases:

1. In the arterial form.
2. For symptomatic (non-idiopathic) nocturnal priapism, when it is necessary to vigorously eliminate the cause of the disease.

Lasting more than three hours out of connection with sexual arousal.

Name

The term "Priapism" comes from Greek mythology, according to which, the god of fertility Priapus (Πρίαπος, Priapus), had a constant erection at any time of the day.

Symptoms

Types of priapism

• Ischemic (accompanied by sharp decline blood flow in the arteries of the cavernous bodies of the penis);
• Non-ischemic, in which there is no disturbance in blood flow;
• Drug-induced - caused by the effect of drugs on the arteries of the cavernous bodies, for example, with injection therapy.

There is also a condition called “pseudopriapism”.

Reasons

Apart from the causes of drug-induced priapism, other factors causing this condition have not been thoroughly studied.

• Non-ischemic priapism can accompany injury to the penis, due to a violation of the insulation between the cavernous bodies and their circulatory system.
• Ischemic priapism can be caused by: inflammatory processes, drug use (the ability to cause priapism is attributed to cocaine), blood diseases such as sickle cell anemia; cancer, spinal cord injuries and side effect medicines.
• Pseudopriapism is a strong nocturnal erection, which is not a pathological condition and does not require treatment.

Prevention of drug-induced priapism

Each patient undergoing testing at the clinic must receive a clinic business card with an emergency telephone number. It is necessary to explain to the patient that in case of an erection lasting more than 4 hours, he must contact the duty officer, regardless of the time of day.
In some countries (Israel, USA), 2 tablets of sinufed (a drug for the common cold containing pseudoephidrine) are used as prophylaxis. This therapy is suggested if you have an erection that lasts more than two hours.

Treatment

Conservative treatment

• immediate cessation of sexual activity until the erection completely disappears;

• If the patient is generally healthy, a cold shower is helpful;
• If cold water is unacceptable from the patient’s point of view, it is necessary to apply ice in a plastic bag to the base of the penis. The procedure lasts about half an hour.
• Physical activity such as climbing stairs, squats, or riding an exercise bike.

• Press firmly on the pubic bone with your thumb for 30 – 60 seconds;

If the erection begins to weaken, it is highly recommended that the patient go to sleep. By morning, as a rule, the penis will be completely relaxed. Sometimes there may be a slight swelling of the corpora cavernosa. This passes in a period from 6 hours to two days;

• If symptoms continue or pain occurs, the patient should report to the clinic for drainage.

Drainage

For drainage you need: kidney-shaped basins, a 20 ml syringe, a 19 G butterfly needle, an elastic bandage, a solution of neosynephrine or its analogues. At Es Class Clinic, it is customary to drain, in contrast to world practice, not by puncturing the head of the penis, but from the lateral side of the penis, a few centimeters from its base.
The penis is disinfected with alcohol and anesthesia is performed with chlorethyl (optional).
Carefully but immediately insert the butterfly needle into the corpus cavernosum until blood begins to flow through the tube into the reniform pelvis.
It is necessary to let the first portion drain. Sometimes this is enough, but in most cases active evacuation of blood from the cavernous bodies is required. Using a syringe, 10-15 ml of blood is evacuated and drained into a basin. Instead, the same amount of neosynephrine solution is injected (diluted 1 to 500), washed with it, followed by evacuation. The procedure is repeated until the pulsating softening of the penis begins. In this case, it is necessary to stop the drainage and wait without removing the needle from the corpus cavernosum. If the erection does not return, it is necessary to remove the needle and bandage the penis with an elastic bandage for 2 hours.  The maximum permissible amount of blood during drainage on an outpatient basis is 500 ml. In case of complicated priapism, when after drainage of 500 ml and lavage there is no effect, it is necessary to send the patient to the hospital. After drainage and dressing, the patient is recommended to rest for half an hour and have sweet coffee. Continuation

Priapism is one of the types of sexual dysfunction, manifested in a persistent, prolonged erection that is not associated with sexual arousal and does not stop after sexual intercourse. As a rule, the development of the disease is associated with blood overflow of the cavernous bodies of the penis. According to the recommendations of the American Urological Association, the temporary criterion for priapism is the duration of an erection for more than 4 hours. Priapism is an urgent urological pathology that requires quick diagnostics and timely treatment.

The etymology of the term "priapism" goes back to the name ancient Greek god Priapus. The latter was revered as the god of fertility and had a huge phallus - a symbol male power. The first mention of the disease in men dates back to the times of the Egyptian pharaohs and is found in the Ebers papyrus. In the era of the development of modern medicine, the first fundamental work devoted to a rare and mysterious disease was an article by Hinman in the Annals of Surgery for 1914. His son, Hinman Jr., hypothesized that venous stasis, combined with increased blood viscosity and ischemia, plays a role in important role in the development of the disease. Burt et al in 1960 first described a case of arterial (non-ischemic, high flow) form of priapism that developed in a young man after injury during sexual intercourse. Another twenty years later, Hauri et al. Using arteriography of the penis and cavernosography, they showed that with this form there is an increased arterial inflow and the absence of ischemic phenomena. Priapism has been associated with urinary infections, pelvic tumors, urinary retention, ejaculation disorders, mental illness, sickle cell disease, thalassemia, leukemia, certain medications, and allergic reactions to insect stings. Despite the fact that over the past twenty years, research into the molecular mechanisms of the pathogenesis of priapism has shed some light on this mysterious disease, the processes underlying its development remain incompletely understood.

Priapism is a fairly rare disease - the incidence is 1.5 cases per 100,000 population per year. The disease occurs in all age groups from newborns to the elderly. When analyzing the distribution of incidence, two peaks are determined - between 5 and 10 years of life in children and 20 and 50 years of life in adults. The incidence of priapism, however, is significantly higher in patients with pathology of the blood system - 29-42% of patients with sickle cell anemia and 50% of patients with CML had one or more episodes of priapism; Some sources suggest that the incidence of priapism in patients with various coagulopathies is also significantly higher than in the population.

Sickle cell anemia is the most common cause development of priapism in childhood, in adults secondary drug priapism, associated with an overdose of drugs for the treatment of erectile dysfunction, comes first. In addition, coagulopathies, neurological diseases, psychoses, tumors of various locations, trauma to the pelvis and perineum can also serve as etiological factors. In more than half of the reported cases, the cause of the disease cannot be determined, then priapism is considered idiopathic. However, in general, the category of greatest risk associated with priapism is considered to be patients with diseases of the blood system. In particular, studies of patients with sickle cell anemia (SCA) have shown that throughout life at least one episode of priapism occurs in 29-42% of patients, and among all patients with priapism, SCA is the etiological factor in 23% of adult patients and 63% of children . In addition to classical SCA, subclinical forms of HbS hemoglobinopathies are also associated with priapism. In the light of a detailed study of the physiology and pathology of the blood coagulation system in recent years Some guesses have appeared about the connection of priapism with direct coagulological disorders. Hinman Jr.'s hypothesis about the factors causing priapism (increased blood viscosity, venous stasis and ischemia) has many similarities with the classical Virchow triad, which determines the factors of venous thrombosis (increased blood coagulability, slow blood flow and pathology of the vessel wall). Analysis of modern data on conditions associated with priapism allows us to find many similarities between venous thrombosis and the ischemic variant of priapism. Cases of priapism have been described in patients with thrombophilic conditions, such as multiple myeloma, leukemia, including chronic myeloblastic leukemia, in which priapism occurs in 50% of cases, asplenism, thrombophilia, erythropoietin therapy, rebound effect after discontinuation of oral anticoagulants. A combination of priapism with hemorrhagic vasculitis - Henoch-Schönlein disease - was observed. Total parenteral nutrition containing 20% ​​fat emulsion has also been associated with priapism. The combination of anticoagulant-deficient thrombophilia with priapism deserves special attention. Proteins C and S are glycoproteins synthesized by the liver with the participation of vitamin K, which, along with antithrombin III and an inhibitor of the tissue pathway of blood coagulation, are components of the natural anticoagulant part of the hemostasis system [I]. Protein C and S deficiency, activated protein C resistance, and antithrombin deficiency are among the most clinically significant thrombophilias associated with a manifold increase in the risk of venous thromboembolism [I]. It is noteworthy that the literature describes cases of both priapism in genuine thrombophilia - isolated deficiency of protein C and a combination of deficiency of its cofactor protein S with SCA - and in latent variants of thrombophilia manifesting while taking oral anticoagulants - warfarin-induced skin necrosis in combination with deficiency protein C or resistance to activated protein C in pediatric and adult therapeutic practice. The mechanism of this phenomenon is explained as follows [I]. Warfarin and other oral anticoagulants exert their pharmacotherapeutic effect by enzymatic inactivation of the vitamin K-epoxide reductant complex. As a result, the synthesis of all vitamin K-dependent proteins in the liver is disrupted, which include procoagulants (blood clotting factors II, VII, IX, X) and anticoagulants (proteins C, S, Z). During warfarin therapy, the levels of all these factors decrease, but procoagulant proteins II, IX, and X have a longer lifespan and their plasma levels decrease more slowly. At the beginning of warfarin therapy, the level of the anticoagulant protein C decreases by 50% in the absence of significant changes in the level of procoagulant factors, which ultimately leads to a hypercoagulable state. In the presence of a previous deficiency of protein C or resistance to activated protein C, a decrease in the level of this anticoagulant during warfarin therapy becomes critical and is clinically expressed in the development of a thrombotic state. The manifestation of priapism may be associated with thrombotic venous occlusion and be a localized manifestation of venous thromboembolism, representing an urgent urological situation. Other blood system pathologies associated with priapism include Olmsted hemoglobinopathy, thalassemia, Fabry fermentopathy. Drugs that are associated with priapism, in addition to oral anticoagulants, include phosphodiesterase-5 inhibitors, prostaglandins, and heparin.

Initially, priapism was classified into primary (idiopathic) and secondary. From the point of view of hemodynamics, two opposite types of priapism can be distinguished - ischemic, also known as low-flow, associated with venous occlusion, and non-ischemic, also known as arterial, high-flow, associated with dysregulation of arteriolar tone and increased arterial blood flow to the cavernous bodies. According to its temporary characteristics, priapism can be divided into acute (a first-time occurrence), intermittent (painful erections lasting about 3 hours, followed by periods of detumescence) and chronic (the latter is usually arterial). According to the recommendations of the American Urological Association, priapism is divided into three types: non-ischemic, ischemic and intermittent.

Non-ischemic (arterial, high-flow) priapism is manifested by persistent erection not associated with sexual arousal due to persistent disruption of blood flow to the corpora cavernosa. At the same time, hypoxemia or acidosis is not observed in the cavernous blood. The penis does not become completely rigid and is almost never painful. Previous perineal trauma is the most commonly reported etiological factor. Arterial priapism does not require urgent treatment. Usually this form ends with the penis returning to a completely relaxed state. Although the increased arterial blood flow in nonischemic priapism was initially thought to correspond to that of normal erection, recent studies have shown that previous trauma causes the formation of fistulas between the cavernous artery and the lacunar spaces of the cavernous tissue, allowing blood to bypass the cavernous flow-regulating resistance of the helical arteries. Non-ischemic priapism, even for many years, may not lead to ultrastructural damage to the cavernous tissue and the development of irreversible changes in it. Based on this, initially conservative tactics using superselective arterial embolization in case of persistence of the disease in most cases allows to achieve the desired result in the treatment of such patients, however, in 11-20% of cases, erectile dysfunction of varying severity is observed after embolization.

Unlike arterial ischemic (veno-occlusive, low-flow) form of priapism is characterized by a sharp decrease or complete absence of cavernous blood flow with pronounced biochemical changes in cavernous blood (hypoxemia, hypercapnia, acidosis). The corpora cavernosa are completely rigid and painful on palpation, and pain is the main complaint of patients. Factors leading to venous occlusion vary depending on the underlying pathology. The ischemic form of priapism is an urgent urological pathology, which, in the absence of treatment, resolves after 24-48 hours by the return of the penis to a relaxed and painless state with a complete loss of erectile function due to cavernous fibrosis in more than 90% of patients. Hinman in his work divided the only ischemic form known at that time into mechanical and nervous subtypes. The mechanical subtype, which accounted for 80% of observations, was correlated with the presence of a mechanical obstruction to the outflow of venous blood from the penis due to thrombosis of the veins of the cavernous bodies, pelvic abscesses and tumors, injuries to the perineum and pelvis, and hematological disorders. He identified the nervous subtype (20% of cases) as priapism due to damage nerve centers regulation of erection. This category included syphilis, brain tumors, epilepsy, intoxication and neurological injury. Hinman Jr. suggested that outflow disturbance and venous stasis were the main reason for the lack of detumescence. This hypothesis was based on the fact that the blood aspirated from the cavernous bodies was viscous, dark and thick, reminiscent of that in other localizations of venous stasis.

The intermittent (recurrent) form is a variant of ischemic priapism, in which episodes of erection lasting about 3 hours are resolved during periods of detumescence, but then reappear, manifesting themselves with the same symptoms (pain and complete rigidity of the penis).

In addition to the three types of priapism discussed, the literature mentions another extremely rare nosological form - partial priapism, or partial thrombosis of the corpus cavernosum, which is clinically characterized by the appearance of a limited painful compaction, usually asymmetrical, in the proximal part of one of the cavernous bodies, after cycling , sexual intercourse, taking marijuana, flying on an airplane and having SCD. No more than 20 cases of this disease have been described in the literature.

The long-noted connection of priapism with the pathology of the blood system has forced us to seek explanations for the role of hematological factors in the pathogenesis of the disease. It is now believed that in sickle cell disease, venous occlusion is the result of a morphological defect in red blood cells containing HbS. The abnormal structure of hemoglobin does not allow red blood cells to be configured in the microvasculature, which leads to venous occlusion and overflow of the cavernous bodies with blood, that is, the development of an ischemic form of priapism. In leukemia, the development of priapism is associated with leukemoid infiltration of the venous bed of the cavernous bodies and direct occlusion of the veins by leukemic cells. In the case of various coagulopathies, the most rational concept seems to be ischemic priapism as a unique form of venous thrombosis associated with the formation of intracavernous thrombi.

The most significant pathogenetic factor determining the prognostic unfavorability of the veno-occlusive form of priapism is cavernous ischemia. According to Kim et al. , in a non-erect state, the partial pressure of oxygen in the blood of the cavernous lacunae is small and amounts to 20-40 mm Hg. Art. During an erection, the influx of arterial blood ensures an increase in oxygen tension to a level of 80-100 mmHg. Art. In the case of arterial priapism, this is what makes it possible to maintain an erection for an unlimited time and the absence of damage to the cavernous tissue. With ischemic priapism, the lack of inflow and outflow of blood from the cavernous bodies leads to a significant increase in hypoxia and accumulation of acidic metabolic products within 4 hours after the onset of the attack, and after 12 hours trabecular edema develops. After 24 hours, if untreated, intracavernous thrombosis becomes complete, and the smooth muscle cells of the lacunae either necrotize or undergo metaplasia into fibroblasts. The latter causes the development of subsequent cavernous fibrosis with loss of erectile function.

Data on the mechanisms of physiological erection and various types of erectile dysfunction suggest that the fundamental factor in the development of erection and detumescence is the tone of smooth muscle cells (SMCs) of the vascular tissues of the penis. The response of smooth muscle cells to an erectile stimulus is determined by the interaction of various psychological and endocrine factors, vasoactive substances, intracellular signaling pathways, down to cellular molecules. It is widely believed that autonomic nervous regulation, the mediators of which are acetylcholine, nitric oxide, cGMP, protein kinase G, norepinephrine, Ras-specific protein kinase, is a fine regulatory string of smooth muscle cell tone. Apparently, the starting point in the pathogenesis of ischemic priapism, in addition to intravascular factors associated with SCA and coagulopathies, may be a violation of the nervous regulation of SMC tone.

In this regard, it would be appropriate to consider the molecular pathogenesis of ischemic priapism using the example of the dosage form of the disease. Drug-induced priapism is a well-known side effect of certain medications and is the most common form of priapism in adults. Kulmlala et al. report that in 21% of cases, priapism is caused by intracavernous injections of vasoactive substances. Papaverine, which inhibits all PDE subtypes and thus blocks the cGMP/PCG and cAMP/PKA signaling pathways, is associated with a risk of priapism in 5% of cases. Intracavernosal injections of PGE1, which blocks only the cAMP/PKA pathway, are associated with a much lower risk of priapism—less than 1% (32). Intraurethral administration of alprostadil and oral administration of sildenafil are comparatively rare cause priapism.

Pharmacological agents change the regulation of SMC tone towards relaxation, which helps prolong the erection. When the penis is in a rigid state, the inflow and outflow of blood is suspended. The partial pressure of oxygen in the cavernous tissue progressively decreases along with erection, so after 4 hours pronounced changes in the gas composition of intracavernous blood occur - hypoxemia and hypercapnia. The lack of oxygen stimulates anaerobic glycolysis with the accumulation of acidic metabolic products; at the same time, blood glucose reserves are depleted, and “local” hypoglycemia occurs. Experimentally, the model of ischemic priapism was recreated in rabbits. The animals were allowed to inhale air with a reduced oxygen content, which led to a systemic decrease in oxygen saturation to 60%, while electrical stimulation of the pelvic nerves was performed. Cavernous ischemia at the cellular level resulted in a significant increase in the activity of myeloperoxidase and lipid peroxidation, as well as in the infiltration of tissues by polymorphonuclear leukocytes. In a model of priapism in dogs caused by intracavernosal administration of high doses of papaverine, local endothelial defects were found, and at the ultramicroscopic level, loss of cell membrane integrity and cytoplasmic condensation. Immunohistochemically, an increase in TGF-? activity was detected. – the main mediator of fibrosis, and in another rat model, neutralization of TGF-? monoclonal antibodies prevented the development of fibrosis after ischemic priapism.

Hypoxia has a significant effect on modulating the effects of endothelin-1 (ET-1) in the penis. Normally, endothelin-1 is expressed by endothelial and stromal cells of the penis and is the most potent inducer of trabecular SMC contraction. According to several sources, the contractile effect of ET-1 is associated with its action on the A subtype of endothelin receptors (ER-A). Activation of another B subtype of endothelin receptors (ER-B), on the contrary, leads to NO-dependent relaxation of SMC trabeculae and other vascular structures. However, during the development of intracavernous hypoxia, endothelin-1 causes relaxation of trabecular SMCs through various counter-regulatory mechanisms, including suppression of Ras-dependent contraction and increase in the amount of ER-B. At the beginning of the development of hypoxia, the level of endothelin-1 increases, this, through ER-A, leads to a decrease in the expression of endothelial NO synthase, which in turn suppresses the cGMP/NO signaling pathway in smooth muscle cells and reciprocally reduces the expression of Ras-specific proteins at the transcription level, which causes a decrease in the contractile ability of the SMC. When hypoxia continues for more than 24 hours, activation of ER-B occurs. Through the formation of nitric oxide, this completes the circle of relaxation of trabecular SMCs. In contrast to the relaxation of arterial SMCs, endothelin-1 causes an increase in venular wall tone through the action of oxygen peroxides, as demonstrated in a rat model. In addition to the effect on venules, aggravating microcirculatory disorders, oxygen peroxides themselves cause damage to cavernous tissue, and the use of allopurinol protects cavernous tissue from this damage in a rat model. Ultimately, hypoxia is caused by endothelin-mediated effects of arteriole relaxation, venule contraction, and cavernous tissue damage.

There is information about a decrease in the sensitivity of β-adrenergic receptors during hypoxia and acidosis. Animal studies have shown that the tone of the SMCs of the cavernous bodies, their spontaneous contractile activity and response to stimulation with β-adrenergic agonists depends on the level of oxygen in the cavernous blood. The lack of contraction of trabecular SMCs upon stimulation of β-adrenergic receptors under hypoxic conditions in vitro is confirmed by the lack of effect from the use of β-adrenergic agonists for ischemic priapism for a long time. Munarriz et al. report that for the treatment of ischemic priapism, high doses of mesatone are necessary to overcome the reduced sensitivity of β-adrenergic receptors. All this suggests that local changes in homeostasis cause a decrease in the tone of trabecular SMCs, which further increases hypoxia and closes the vicious circle.

When using certain medications, the primary point of action is the relaxation of the SMC and an increase in the duration of erection, which, leading to metabolic disorders in the cavernous bodies, contribute to a further decrease in vascular muscle tone and the development of the clinical picture of priapism. With the development of priapism in combination with hematological diseases such as SCA, leukemia and coagulopathy, primary veno-occlusion is not associated with a violation of the tone of the SMC. However, the molecular vicious circle remains the same, only starting from the other side: venous stasis leads to hypoxia, which, due to the action of a number of factors, causes relaxation of trabecular SMCs, an increase in blood flow and further progression of cavernous hemodynamic disorders.

Other possible molecular mechanisms for the development of priapism have been found: dysfunction of phosphodiesterase-5 and dysregulation of NO synthesis. Thus, in the second study, it was shown that insufficient secretion of nitric oxide leads to the development of priapism in mice, and restoration of secretion by intracorporeal injection of a vector with a normal gene corrects the manifestations of the disease. Changes in the activity of endothelial and neuronal NO synthases may be the cause of idiopathic priapism.

Diagnosis of priapism is usually not difficult due to the characteristic picture of the disease, including a prolonged (more than 4 hours) erection, not associated with sexual arousal and in most cases accompanied by pain in the penis. The key point in diagnosis is the determination of the hemodynamic form of priapism, since this is what determines the prognosis of the disease and treatment tactics: veno-occlusive priapism, due to the ischemic nature of damage to the cavernous tissue, requires urgent intervention, in the absence of which the likelihood of maintaining normal erectile function progressively decreases over time. During a survey and physical examination, differential diagnostic signs may include pain (only in the ischemic form), the degree of penile rigidity (full in the ischemic form) and anamnestic data (trauma is more typical for arterial form, diseases of the blood system - for the ischemic form). When examining the penis, pay attention to the presence or absence of rigidity of the spongy tissue. Examination of the perineum, abdomen and rectal examination can help identify signs of previous trauma.

However, only laboratory and instrumental methods can reliably distinguish the ischemic form of priapism from the non-ischemic one, which include gas analysis of cavernous blood aspirate, cavernosography, scintigraphy and duplex ultrasound of the cavernous bodies. It is the latter that is the “gold standard” for the differential diagnosis of forms of priapism, which makes it possible to non-invasively and at the same time reliably determine the hemodynamic form of priapism and determine the need for intracavernous manipulations. Ultrasound signs of veno-occlusive priapism include minimal or zero blood flow velocity in the cavernous arteries and the absence of blood flow in the cavernous bodies (Fig. 1). With arterial priapism, blood flow in the cavernous arteries is normal or increased, but blood flow is present in the cavernous bodies. Duplex scanning is performed in a lithotomy position, the perineal area is examined, and then the entire shaft of the penis from the root to the head. With non-ischemic priapism of traumatic origin, arteriovenous fistulas and pseudoaneurysms are often identified in the perineal sections of the cavernous bodies (Fig. 2-4). If it is impossible to perform an ultrasound, they resort to puncture of the corpora cavernosa with aspiration of blood and analysis of its gas composition. Aspirate from ischemic priapism is dark in color (see Fig. 6), the partial pressure of oxygen is less than 30 mm Hg. Art., carbon dioxide - more than 60 mm Hg. Art., pH – less than 7.25.

The management of arterial priapism is generally conservative. If ultrasound does not reveal significant damage to the cavernous vessels, the tactics for managing these patients is dynamic observation; in most cases, spontaneous remissions occur. In the absence of resolution of the disease and the patient's desire, superselective embolization of cavernous vessels is used, which is currently the most widely used and effective method treatment of arterial priapism, however, as noted above, is associated with a risk of erectile dysfunction. Access is made standardly through the femoral artery, after which arteriocavernosography is performed (Fig. 5). Absorbable and non-absorbable (permanent) materials can be used as occluding agents. The first includes autologous thrombotic masses and gelatin microspheres, the second - spirals, ethyl and polyvinyl alcohol, acrylic microspheres. The effectiveness of absorbable and nonabsorbable agents is reported to be comparable (74% vs. 78%), with the use of absorbable agents associated with a significantly lower risk of postoperative erectile dysfunction (5% vs. 39%). When embolization is ineffective and large arteriovenous fistulas are present, cases of open revision and ligation of vascular malformations have been described - the effectiveness of the method was up to 63%, but almost half of the patients had severe erectile dysfunction after surgery. Due to the rarity of the disease, the available data are from descriptive studies in a small number of patients, and there have been no controlled trials of different treatment regimens (observation, embolization or surgical ligation).

Treatment of the veno-occlusive form of priapism is carried out according to urgent indications. Under local anesthesia (dorsal nerve block), the corpora cavernosa are punctured and blood is aspirated from them. Traditionally, the lateral approach is in the middle part of the shaft of the penis at 3 or 9 o'clock, providing the best opportunities for aspiration and irrigation of cavernous lacunae (Fig. 6). Usually, after a puncture, the blood begins to spontaneously separate through the needle. In cases of recurrent attacks of priapism or the presence of cavernous fibrosis, active aspiration may be necessary. The collected blood is sent for biochemical testing to confirm the diagnosis. If more than 24 hours have passed since the onset of the attack, with repeated episodes of priapism and drug priapism after intracavernous injections after aspiration of blood, it is recommended to irrigate the cavernous lacunae with an isotonic solution of sodium chloride. To do this, in addition to installing an aspiration needle in the middle part of the shaft, it is necessary to install an irrigation access closer to the base of the penis (Fig. 7). Resolution of an attack of priapism after aspiration and irrigation is observed in 30% of patients. The puncture site must be subjected to compression for 30-60 minutes to prevent the formation of a hematoma. As alternative approaches, it is possible to use transgladular puncture, which reduces the risk of hematoma development, and also makes possible cavernous-glandular shunting of blood after removal of the needle (according to Winter, see below), or puncture of the cavernous bodies in the area of ​​the legs and distal part. If there is no effect from aspiration and irrigation, sympathomimetics are injected intracavernosally through a butterfly needle, which promotes the development of detumescence. Phenylephrine (Mesatone) is commonly used due to its selective effect on alpha-1 adrenergic receptors and minimization of cardiovascular risks. The dosage regimen of the drug is 100-150 mcg every 5-10 minutes before detumescence occurs. The maximum dose is 1000 mcg. In this case, the disappearance of priapism is observed in 43-81% of patients.

Surgical treatment of ischemic priapism is performed in the absence of spontaneous detumescence and the absence of effect from conservative measures. The essence of the operations used (Fig. 8) is to restore impaired venous outflow by creating artificial cavernous-venous shunts. More preferable is the creation of distal (cavernous-glandular) anastomoses - according to Winter (with a biopsy needle), according to Ebbehoy (percutaneously with a scalpel) and according to El-Gorab (creating a hole in the tunica albuginea of ​​the distal part of the cavernous body). The restoration of blood flow and the functioning of the shunt in this case can be easily checked by ultrasound (Fig. 9). If there is no effect from distal anastomosing operations, proximal anastomoses are applied between the pedicles of the corpora cavernosa and the proximal part of the corpus spongiosum (according to Kvokel-Setcher) and saphenocavernous anastomosis according to Greyhack. These procedures are less preferable due to the risk of developing serious complications: Kwokel-Setcher anastomosis is associated with urethral fistulas and purulent cavernositis, Grayhack anastomosis is associated with pulmonary embolism.

Penile prosthesis is actually a treatment for complications of priapism - developed complete erectile dysfunction that is refractory to drug therapy. One study from the London Institute of Urology presented data on 8 patients with an acute attack of ischemic priapism of various etiologies. Conservative therapy was ineffective in all patients; in half of them, priapism attacks were recurrent after bypass surgery. The ischemic nature of the disorders was confirmed by Doppler scanning data and gas analysis of cavernous blood aspirate. All patients underwent penile prosthetics, 6 of them with semi-rigid prostheses and two with inflatable three-component ones (Fig. 10). The average postoperative follow-up period was 17 months (from 5 to 35), 7 out of 8 patients had satisfactory sexual function, one did not have a sexual partner, which made assessment of the functional outcome impossible. Tamella substantiates the inevitability of cavernous fibrosis after 24 hours of an attack of priapism. Sundaram et al. describes the story of a 40-year-old patient with refractory priapism, in whom penile prosthesis was preferred over shunt surgery. When choosing a method of surgical treatment of priapism (shunt surgery or prosthetics), it is necessary to be guided by the duration of the attack of the disease. If it lasts less than 24 hours, it is possible to preserve erectile function to some extent and it is possible to perform shunt surgery to resolve the attack. If the attack lasts more than 24 hours, the likelihood of cavernous fibrosis occurring is very high and shunt operations will only stop the attack, but will not lead to the restoration of erectile function. In this case, you should immediately give preference to penile prosthesis. This treatment method is often used in patients with high risk the occurrence of repeated episodes of the disease (for example, with SCD), when prostheses are installed immediately after aspiration and irrigation.

One of the most difficult and unresolved issues to date is the treatment of recurrent forms of priapism. Being ischemic in nature, it determines the doctor’s prognostic alertness in terms of the development of erectile dysfunction; at the same time, spontaneous relief of episodes lasting less than 3 hours shifts the main emphasis in the treatment of this pathology to secondary prevention, that is, prevention of relapses of the disease, which is essentially a conservative treatment of intermittent priapism during remission. During attacks of intermittent priapism therapeutic tactics remains the same as with any other variants of ischemic priapism.

Levine and Guss report the successful use of a GnRH analogue in a patient with SCD and recurrent priapism for a year. Similar data are reported by Steinberg et al. . A 32-year-old patient with recurrent priapism (but without SCA) was initially trained in the technique of intracavernosal injections of adrenaline; however, he needed a more comfortable form of drug administration while maintaining libido and sexual function. Leuprolide 7.5 mg was administered once a month. The patient did not notice a decrease in libido for two months. Four months after discontinuation of therapy, the patient's erections were sufficient for sexual intercourse, but he did not report episodes of prolonged painful erections. Dahm et al. report the use of bicalutamide in 3 patients with a combination of SCA and refractory recurrent priapism. It is noteworthy that despite the absence of a decrease in libido and sexual function, significant improvement during the course of the disease was detected in all patients. Similar data with no decrease in erectile function are confirmed in a study by Hoffman et al. , where bicalutamide was combined with a β-agonist and Costabile, which used flutamide orally at a dose of 125 mg 3 times a day. Yamashita gives a case report of a 56-year-old patient with recurrent priapism. Initially, the patient took 50 mg of chlormadinone daily in combination with intracavernous injections of an adrenergic agonist. Due to the lack of effect, the dose of chlormadinone was increased to 100 mg, as a result of which the level of total testosterone dropped to 0.43 ng/ml and erectile dysfunction developed, and therefore treatment was discontinued. However, after discontinuation of the drug, erectile function gradually returned to its original level and no more episodes of priapism were observed. Serjeant et al. conducted a double-blind, placebo-controlled crossover study on the use of silbestrol in patients with a combination of SCA and recurrent priapism. According to the study results, the drug at a dose of 5 mg daily led to a significant reduction in the frequency of attacks compared to placebo. However, the number of patients in the study (11 people) was not enough to form clear conclusions about the possibility of using estrogens in these patients. Compared to antiandrogens, the use of estrogens is less preferred because they are associated with an increased risk of VTE, obesity and gynecomastia. In general, the use of hormonal therapy for priapism remains empirical - there are no studies that clearly establish the influence of testosterone levels on the course of recurrent priapism.

Baclufen is a GABA receptor agonist and inhibits reflexes at the spinal level by hyperpolarizing afferent terminals. Some studies have shown that baclofen may inhibit erection and ejaculation. In a study by Denys et al. 9 patients received baclofen for the treatment of spastic paresis (etiology: spinal cord injury and multiple sclerosis). 8 of them had ED of varying severity with a median follow-up of 44.4 months. Abrupt withdrawal of baclofen has been shown to provoke a withdrawal syndrome with the development of priapism. Vaidinaythan et al report a 46-year-old patient with spinal cord injury at the C4 level. 12 weeks after the injury, he developed recurrent priapism, with attacks of the disease being triggered by the slightest movement. During therapy with baclofen at a dose of 10 mg 3 times a day, the frequency and duration of episodes began to steadily decrease. The same results were obtained by Rourke et al. : When baclofen was administered at a dose of 40 mg per day, a 41-year-old patient with nocturnal recurrent priapism experienced complete resolution of symptoms. Observation for a year after discontinuation of therapy showed persistent preservation of the effect with normal sexual function.

Perimenis et al. showed the effectiveness of the anticonvulsant gabapentin in three patients with idiopathic priapism. Two patients had no episodes of priapism while continuing low-dose therapy for 16 and 24 months, respectively. The third patient, after successful treatment for 6 months, stopped taking the drug and had a relapse of the disease. After resumption of therapy, he again experienced remission (follow-up period - 9 months). It is possible that the mechanism of action of gabapentin is associated with suppression of the release of calcium ions from trabecular SMCs and suppression of their relaxation. Additionally, gabapentin has been shown to significantly reduce testosterone and FSH levels in rats.

Selective? The 2-adrenergic agonist terbutaline showed its effectiveness in the work of Ahmed et al. in the treatment of recurrent priapism in an 11-year-old boy. Therapy at an initial dose of 3 mg followed by a decrease to 1.5 mg over one week resulted in the disappearance of attacks for 6 months. In a placebo-controlled study of the effectiveness of terbutaline in the treatment of patients with PGE-induced priapism, detumescence occurred in 36% of patients compared with 12% in the placebo group. These results suggest that terbutaline may be used as initial therapy for drug-induced priapism. According to recent studies, the pathogenesis of priapism includes a decrease in the amount of PDE-5 in the cavernous tissue, which, leading to an increase in the level of cGMP, promotes relaxation of trabecular SMCs. Interestingly, in 2002, Bialecki and Bridges reported relief of acute attacks of priapism and a reduction in the frequency of relapses in patients with SCD when taking sildenafil 50 mg. Long-term use of the drug in mice deficient in endothelial NO synthase led to an increase in the amount of PDE-5 and a decrease in episodes of priapism. Burnett et al. used sildenafil at a dose of 25 mg daily with a further transition to tadalafil at a dose of 5 mg three times a week in a group of patients with SCD and obtained a long-term remission, and before starting therapy, patients tried all available methods of pharmacotherapy without effect. Thus, low-dose PDE5 inhibitor therapy is paradoxically effective for priapism, but the effectiveness of this treatment method requires further study.

Some drugs may not be used for systemic therapy, but for independent intracavernous injections. McDonald and Santucci report the successful treatment of a patient with heterozygous HbS hemoglobinopathy and recurrent priapism with metaraminol (selective β-adrenergic agonist) at a dose of 5-10 mg once a week as an intracavernous injection. Complete detumescence was observed 3-10 minutes after injection. Another drug that can be used for self-administration is etilephrine, which also belongs to the selective β-adrenergic agonists. Teloken et al describe the experience of using the drug in a 27-year-old man with intermittent idiopathic priapism for 1 year. Terbutaline therapy was ineffective, and therefore intracavernous irrigation with drainage and administration of 5 mg etilephrine was performed, resulting in detumescence. Subsequently, the patient was trained to self-administer the drug at a dose of 5 mg when the attack lasted more than 1 hour. After a month of treatment, remission was achieved, at the same time, sexual activity was fully preserved.

A common disadvantage of intracavernous injections is a certain complexity and inconvenience of a technical nature, which cannot be overcome by all patients. Other possible complications include possible infection and scarring. Ralph et al describe the experience of using an implantable delivery system (IDS) of mesatone in a 28-year-old patient with a 3-year history of recurrent priapism. Through a lateral penoscrotal incision, a system was implanted with a cannula inserted from the lateral side into the right cavernous body and fixed with non-absorbable sutures. The reservoir was placed under the skin of the scrotum. After the initial titration, a dosage regimen was selected - 50 mg of mezatone in 8 ml of ICN was percutaneously injected into the reservoir once every two weeks. If intracavernous injection was necessary, the patient could simply press the pump button - one press provided the infusion of 0.1 ml of solution. As a result of using ISD for 4 months, all incipient attacks were immediately stopped.

Alteplase or tissue plasminogen activator (tPA) is a 2nd generation thrombolytic drug, a serine protease that converts plasminogen to plasmin. Even in Hinman’s article, it was suggested that priapism develops as a result of thrombosis of the cavernous veins, and those given in this review data confirm the connection of the disease with hypercoagulable states. The effectiveness of thrombolytic therapy in thrombotic processes such as myocardial infarction and ischemic stroke has been known for a long time [I]. In their article, Rutchik et al. discuss the successful use of a single intracavernous injection of alteplase in a 35-year-old patient with recurrent priapism and a frequency of attacks twice a day. Aspiration with irrigation of the cavernous bodies, intracavernous administration of mesatone, and even surgical treatment - El-Gorab shunting - were carried out without effect. After administration of 15 mg of alteplase into the right cavernous body during one of the attacks, almost complete detumescence was observed within 15 minutes. The use of alteplase has a pharmacokinetic advantage over other thrombolytics due to its low half-life (about 5 minutes). However, thrombolysis cannot be performed by the patient at home due to the risk of life-threatening bleeding. Methylene blue is a guanylate cyclase inhibitor. It blocks NO-mediated relaxation of trabecular SMCs. The effectiveness of intracavernous injection of the drug has been shown in rats, rabbits, and humans in the treatment of all forms of priapism. However, there have been no studies on the direct effect of methylene blue on the course of recurrent priapism.

Despite the popularity and more than a century-long history of studying priapism in modern medicine, it still remains a serious, urgent and at the same time rare and insufficiently studied urological pathology. Identification of hemodynamic forms of priapism made it possible to take significant steps in the correct management of patients. The role of hematological and coagulation disorders as the main cause of idiopathic priapism has been established. New data on the connection of the disease with an imbalance in the regulation of trabecular SMC tone have made it possible to somewhat clarify the pathogenesis of the disease and characterize the universal nature of microcirculation disorders and the level of cellular substrates in various etiologies of priapism. Perhaps further study of the role of molecular factors in the mechanism of development of priapism will make it possible to create effective and safe drugs for its treatment. Currently, invasive manipulations and surgical techniques play a leading role in the treatment of most forms of priapism. Although the use of various groups of drugs for the secondary prevention of recurrent priapism has been described, due to the lack of a significant number of observations, there is no evidence base for the choice of one or another pharmacological agent or method of intervention. It is hoped that in the future, the use of experience and the accumulation of new data in studies with the correct design and sufficient statistical power will help modern urology to solve the problem of the mysterious phenomenon of priapism.

List of abbreviations:

VTE – venous thromboembolism

SMCs – smooth muscle cells

GnRH – gonadotropin-releasing hormone

ISD – implantable delivery system

ICN – isotonic sodium chloride solution

PGE – prostaglandin E

PKA – protein kinase A

PKG – protein kinase G

SCA – sickle cell anemia

TFR-? – transforming growth factor – beta

PE – pulmonary embolism

FSH – follicle stimulating hormone

CML – chronic myeloid leukemia

cAMP – cyclic adenosine monophosphate

cGMP – cyclic guanosine monophosphate

ET - endothelin

ER-A – endothelin receptor subtype A

ER-B - endothelin receptor subtype B

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When it comes to men's health, erection problems and impotence are most often thought of. But there are also opposite conditions, when the penis is in an excited state for a long time.

Priapism is a disease characterized by prolonged and painful erections that are not associated with sexual arousal. In a normal state, the erect penis returns to its original size shortly after ejaculation, and completed sexual intercourse brings pleasure. In a painful state, an erection does not go away for 4-6 hours.

This pathology is quite rare, but if its symptoms appear, you should immediately seek medical help. It is impossible to get rid of priapism without special manipulations and procedures; no folk methods will help in this case. If you ignore the alarming symptoms, the man’s condition may worsen so much that amputation of the penis is required.

Features of the disease

When a man really wants to have sexual intercourse, complex processes are launched in his body that lead to arousal. An erection occurs after the smooth muscles of the penis are completely relaxed and fluid flows into the cavernous bodies. arterial blood. As a result, the penis increases in size and becomes hard.

The penis will remain in an excited state as long as the cavernous bodies compress the veins, interfering with the outflow of blood. The logical conclusion of sexual intercourse is ejaculation and orgasm, after which the cavernous bodies stop blocking the outflow of blood through the veins. The penis shrinks and becomes soft.

With priapism, the process of blood outflow from the cavernous bodies of the penis is disrupted, and an erection persists for a long time. Soon it becomes painful, and the penis acquires a bluish tint.

Manifestations of the disease may differ slightly depending on the type of pathology:

1. Ischemic priapism – the outflow of blood from the penis is completely absent. In this case, the erection lasts at least 4 hours. She is not related to sexual desires men, continues even after sexual intercourse. The body of the penis is very hard, and the head is soft, due to the difference in pressure, the penis bends towards the stomach. The ischemic form of the disease can be recurrent or irreversible. In the first case, a prolonged erection occurs from time to time, its duration is less than 3 hours. The irreversible form of priapism is especially dangerous and requires immediate medical attention.
2. Non-ischemic priapism is characterized by the presence of a slight outflow of blood. The erection in this case will be just as long-lasting, but the penis will not be painful and will be softer than with the ischemic form of the disease.

In addition, there is false priapism. This is the name for involuntary nocturnal erection, which has nothing to do with true priapism, which is a serious disease.

You can get more detailed information about this problem from the video, where experienced specialists talk about the features of the disease and modern ways treatment.

Cases of prolonged painful arousal can also be observed in women. Female priapism manifests itself in an enlargement of the clitoris (up to 2 cm), it becomes painful and changes color. Even in the absence of physical or psychological stimulation, the clitoris does not decrease in size. This condition can last from several minutes to several days.

The female type of pathology and male priapism are similar Their origins are pathological processes that cause disruption of blood flow in the human genital organs.

Prostate inflammation

The main cause of painful and prolonged erection is stagnation of blood in the cavernous bodies of the penis. The blood circulation process can be disrupted due to the negative effects of various factors. One of them is inflammation of the prostate.

The prostate gland is responsible for:

• sperm quality. Prostatic juice is synthesized in the prostate gland - this liquid forms the basis of sperm;
• actively participates in the process of ejaculate release during sexual intercourse;
• directly responsible for bringing the penis into an excited state and achieving orgasm;
• controls the process of blood supply to the penis and other organs of the male genitourinary system;
• forms hormonal balance men, since it is in the prostate that testosterone becomes active.

Inflammatory processes occurring in the prostate gland are commonly called prostatitis. Typically, this disease causes a man to have difficulty getting an erection. Due to poor circulation, the cavernous bodies of the penis are not filled sufficient quantity blood, and, therefore, an erection does not occur.

But sometimes inflammatory processes in the prostate block blood flow in such a way that the blood-filled cavernous bodies cannot empty, and the penis continues to be erect for several hours.

Other causes of priapism

Priapism can occur at any age. There have been cases of this pathology in boys 5-6 years old, as well as in mature people whose age is 45-50 years. The following factors can provoke the disease:

1. Injuries affecting the base of the penis.
2. Oncological diseases.
3. Pathological processes that have a negative impact on the blood vessels located in the lumbar and coccyx areas.
4. Blood diseases.
5. Intoxication of various natures, including drug overdose, alcohol abuse, etc.
6. Diseases that are infectious in nature, such as rabies and typhus.
7. Decompensated renal failure.
8. Forced sexual arousal for a long time.

Priapism can develop against the background of psycho-emotional trauma received by a man during sexual intercourse. Some medications can lead to this condition. Among them are strong psychotropic drugs, antidepressants, sedatives, anticoagulants with indirect action, as well as drugs that can help achieve a temporary erection.

Treatment

On the Internet you can find several videos with recipes for treating priapism. But the truth is that you can only get rid of this condition with the help of doctors. All a man suffering from priapism can do at home is apply cold to the excited organ. Further treatment will be carried out by doctors within the walls of the medical institution.

Treatment can be carried out in several directions:

• Drug treatment involves injecting drugs into the man’s penis that can thin and remove blood. Punctures are carried out in combination with taking anti-inflammatory and painkillers. As a result, the amount of blood in the cavernous bodies of the penis decreases, and the man’s condition improves. At the same time, it is necessary to identify the cause of priapism as quickly as possible and begin treatment of the underlying disease;
• Surgical treatment is carried out if drug therapy has been ineffective. Surgery will also help with relapses of the disease. During the operation, doctors normalize blood flow and remove individual blood clots;
• In some cases, only amputation of the penis can cure priapism. Such radical measures are taken in as a last resort when the disease is in an extremely severe stage or in the presence of cancer.

One of the complications of such a disease as priapism is impotence. Loss of the ability to have a normal erection occurs due to the development of cavernous fibrosis.

Despite the fact that it is not recommended to treat priapism using traditional methods, there are still several ways to alleviate the patient’s condition before providing medical assistance. Applying ice packs will slightly lower blood pressure in the groin area. A similar effect can be obtained by performing sports exercises included in the step aerobics complex. You can use the nearest ladder as a sports equipment.
Priapism is a fairly rare disease, but in order to completely exclude the possibility of its development, you should regularly undergo examination by a doctor specializing in the treatment of diseases of the male genitourinary system. In addition, you should lead an active lifestyle, avoid excessive drinking and streamline your sex life. If you have diseases that can lead to long-term painful erections, it is important to treat them promptly. Men who suffer from sickle cell anemia should be especially careful.