Lecture on hamoglobinuria

2021-01-31 12:00 AM

Deposits in the renal tubules (hemoglobin, tubular epithelial cells) can block the renal tubules, preventing urinary excretion.

Define

Hemoglobinuria is a serious malaria disease caused by acute red blood cell breakdown that causes acute anemia, acute renal failure, jaundice-mucosal jaundice and many other disorders. If not treated properly and promptly, it will lead to death.

Mechanism of pathogenesis

The mechanism of rupture of erythrocytes

Because malaria itself is severe

This leads to severe rupture of erythrocytes and hemoglobinuria, also known as "spontaneous" hemorrhagic malaria (without the involvement of malaria drugs). The likelihood mechanism is due to the following factors:

Increased macrophage activity against both parasites and erythrocytes.

Mechanism of attachment of parasitic infected red blood cells to the endothelium of the vessel wall.

The autoimmune mechanism due to the formation of autoantigens from erythrocytes changes the membrane structure, from which autoantibodies appear.

Due to the role of the drug

Many drugs, including the drug malaria, can cause erythropoiesis and are divided into three groups:

The group of drugs that cause complications in everyone: Sulfone, Phenyl hydrazine, acetyl phenyl hydrazine.

The group of drugs causing complications in people with unsustainable haemoglobin such as sulfamid, 4 aminoquinoline.

The group of drugs causing complications in people lacking the enzyme G.6.PD such as: Quinine ranks first, followed by primaquine, mepacrine, amidopyrine ...

Stemming from the two above mechanisms, hemoglobinuria is now divided into 2 types:

Malaria patients with hemoglobinuria due to the development of malaria itself: This type of hemorrhagic malaria often arises in severe, recurrent malaria cases due to P. falciparum, this type the variable is usually heavy and very heavy.

Malaria patients with haematuria caused by factors of malaria drugs, the leading is quinine: This type of hemorrhagic malaria can occur in all patients with severe and mild malaria, progressing not massively. as intense as the above type.

Mechanism of hemoglobinuria

Malaria more or less has broken red blood cells, but not everyone has hemoglobinuria. When hemolysis there will be hemoglobin in the blood plasma; Normally 1 liter of plasma has enough haptoglobin to fix 1 g of hemoglobin in the blood plasma; this hemoglobin count will be converted to 40mg bilirubin by endothelial reticulocytes in the liver; When mass hemolysis with hemoglobin greater than 1.35 g in 1 litter of plasma, 1g of hemoglobin will be fixed and converted to bile pigment, leaving 0.35g free hemoglobin in the blood The plasma is a small part is fixed by the plasma albumin to methemalbumin and the remaining free hemoglobin will be excreted through the kidneys in the urine; The renal clearance to hemoglobin is: 6 ml of plasma for 1 minute with haemoglobin concentration of 2-3 g / litter of plasma. Thus, haemoglobinuria only occurs in malaria patients when the patient has a strong haemolytic process; impaired hepatic endothelial reticular tissue is an advantageous factor because it is unstable and converts haemoglobin into bilirubin; Renal failure will prolong the excretion of haemoglobin in the urine.

Mechanism of acute renal failure

Patients with haemoglobinuria are more susceptible to physical acute renal failure because:

Massive haemolysis with acute anemia and hypoxia causes tubular necrosis and disturbances of tubular absorption; on the other hand, acute anemia causes blood vessel spasm reflexes and hemodynamic disorder with decreased glomerular filtration; Both types of damage to the kidney tubules and glomeruli lead to acute renal failure: Primary, anuria, in which anemia - renal tubular hypoxia is the main.

Deposits in the renal tubules (haemoglobin, tubular epithelial cells) can obstruct the renal tubules, prevent urinary excretion, but this obstruction is only a secondary, secondary, no basic.

In addition, haemoglobinuria in the first 1-2 days may present with acute functional renal failure due to dehydration (due to vomiting, excessive sweating ...).

clinical

Onset

Usually suddenly, the patient has chills, high fever, headache; pain across the back and spine, often vomiting a lot green - yellow or gagging fluid; mucosal skin turns pale green quickly, sometimes jaundice and early eyes; dark brown urine such as coffee or thick water; Patients often struggle, panicking because of acute lack of oxygen.

Includes the following main symptoms:

Fever becomes seized, vomiting, back pain.

Hemolytic jaundice.

Hemoglobinuria.

Acute anemia and hypoxia.

The patient continued to have a high fever accompanied by chills. Each chills and fever are often accompanied by a haemolytic episode. Continued vomiting of yellow-green stomach fluids and bile. Sweating a lot. Rapid dehydration and electrolyte disturbances.

Jaundice and mucous membranes appear from the end of day one. After each fever and malaria, the yellow color increases again, becoming dark yellow. There are also cases of unknown jaundice (when the haemolysis is mild or the patient's skin is brown).

Hemoglobin urine: At first often reddish brown, later turning black like condensed coffee or thick water because oxyhemoglobin converts to methemoglobin.

Anemia, acute hypoxia: Due to acute and massive haemolysis, the patient has symptoms of acute hypoxia such as pale green mucous skin, or dizziness, dizziness, dizziness, rapid pulse, knife blood pressure moving, shortness of breath, sometimes chest tightness, restlessness, always anxious on the bed, struggling, panic.

Test

Plasmodium

Before haemolysis, malaria parasites can be seen in 75% of cases, but after the episode, only 1 / 4-1 / 3 cases, because many parasitic erythrocytes were broken.

Blood

Fast and severe anemia, in the first day the red blood cells may drop to 1-2 million / mm3 or less, the haemoglobin also decreased. After the haemolysis is over, the blood quickly recovers with signs of regeneration such as: Appearance of young erythrocytes, with alkaline dots, reticulocytes increased. In the case of dehydration, shock, and aneurysms can cause her blood, haemoglobin and red blood cells to artificially increase. The leukocytes usually increase, averaging about 15,000 / mm3, sometimes up to 40-50,000 / mm3 or more, the formula turns left clearly.

Urine

Proteinuria is usually 4 -5 g / l; Urea and Cl- urinary decrease due to tubular failure; has many erythrocyte pigments such as oxyhaemoglobin especially methaemoglobin and bile pigment like urobilin.

Other tests

Indirect increase in bilirubin in the blood; serum iron increased to 200-300g%; blood urea is always 16 - 80 mmol / litter high, usually very high in the presence of acute renal failure; Potassium is usually high with low urination and physical acute renal failure. Usually there is acidosis with low pH, low alkaline reserve of about 40-30mmol / litter. SGOT and SGPT enzymes are high in some severe cases, when both direct and indirect bilirubin is high.

Developments

The case goes well

The fever goes away quickly, the haemolysis is only 1-2 times and then goes away, the urine fades, returns to normal from day 6 to day 10, red blood cell pigment (haemoglobin) and bile pigment (bilirubin, urobilin) gradually decreased, jaundice gradually faded in parallel with decreased blood bilirubin, erythrocytes increased, blood urea also gradually returned to normal. Recovery takes about 1 month.

The case goes bad

 The fever continued every day with chills, haemolytic episodes recurred every day at the time of the fever, jaundice increased, red blood cells decreased, urine continued to dark brown, the number gradually decreased. 200-400 ml to 40-50ml in 24 hours, even on days of complete anuria, urea increased, the patient turns into acute renal failure, increased blood K +, metabolic acidosis appears, awake the patient, overcast, even in a coma. There are also cases of patients with acute circulatory failure, or acute liver failure, or transitioning to an acute encephalopathy due to cerebral hypoxia.

Complications, prognosis, death

Symptoms

Acute renal failure

The most common and dangerous complication, which can appear early, is usually functional acute renal failure due to water deficiency, with high haematocrit, low urination, but urea, creatinine, and Na + clearance are normal; This type is usually mild. From day 4 onwards, acute renal failure is more likely to be due to tubular necrosis: minimal, anuria about 30-100ml / 24 hours, blood urea increased> 7.3 mmol / l, urea is lower than average Usually (<250mmol / 24 hours), creatinine clearance decreases, K + increases by more than 5mmol / l. The patient gradually turns into metabolic acidosis (Kussmaul breathing, Cheynes Stokes), urea poisoning (bloody stools, small pupils, vomiting, gloominess, coma), hyperkalaemia (bloating, paralysis intestinal, low blood pressure, electrocardiogram with symmetrical spike high T waves, wide QRS, loss of P ...), threatening cardiac arrest.

Cardiovascular, circulatory failure

Low blood pressure and rapid pulse are also a common complication due to haemolysis or dehydration and salt causing acute kidney failure and hyperkalaemia. 

Acute brain syndrome

Due to severe haemolysis causing cerebral hypoxia (8.4%), or due to hyperaemia coma (5.6%).

Complications in the liver bile

The SGOT and SGPT enzymes are elevated, and the patient has an acute liver failure due to acute hepatic parenchymal necrosis.

Prognosis

Symptoms have prognostic significance

Mental state.

Red blood cell count.  

Malaria and haemolytic again.

Vomiting and sweating a lot.

The amount of urine.

 Classification according to prognosis

Signal

Fit

Heavy

Very heavy

Neuropsychiatric

stability

Flustered, struggling, anxious, panic

Overcast, sunset

Respiratory, circulatory

stability

100 rapid pulse, shortness of breath, fluctuating BP

Pulse 100, small, shortness of breath, rapid, shallow, hypotension

Digestive

No vomiting, little vomiting

Vomiting moderate

Vomiting, loose diarrheal, bloating, hiccups

Blood

Red blood cells 2T-3T

Erythrocytes 1-2T large interval of erythropoiesis

erythrocytes <1T large erythrocytic distance

Urine

500-1000ml/ 24giờ,

light brown

<500 ml / 24 hours, dark brown

<100ml / 24hours, dark brown

Fever and haemolysis

Fever 38 ° C

Light burning

1-2 episodes of haemolysis

High fever 39-40 ° C Shivering

3-4 haemolysis

High fever 39-40 ° C Shivering for many days, 5 or more haemolytic attacks

Jaundice

Bilirubin blood

Urea of ​​blood

Light

£ 85 m mol / litter

7-17 mmol / litter

Fit

> 85 - 170 m mol / litter

> 17-50 mmol / litter

Dark

> 170 m mol / litter

> 50 mmol / litter

Dead

The direct cause of death is usually

Acute renal failure leads to high blood protein, high blood K +, and cardiac arrest.

Seizure coma due to lack of brain oxygen or high blood protein, breathing failure.

Cardiomyopathy, hypotension due to water electrolyte disturbance, "hemolytic" shock, or myocardial failure due to lack of oxygen or hyperkalaemia.

Diagnosis of hemoglobinuria

Suspected symptoms

Malaria patient has moderate fever, suddenly has a high fever, before only a mild cold, suddenly there is a shivering cold.

Vomiting a lot of "green honey, yellow honey".

Very pain in the back, pain along the spine, pain in the lower ribs.

Skin pale green mucous very quickly, yellowish in eyes appears.

Ending struggling, struggling in bed, feeling dizzy, flustered and panicking every other day.

Urination feels hot foreskin (in some patients).

When encountering these suspicious signs, it is necessary to immediately observe the urine, check the hemoglobinuria.

Diagnosis of hemoglobinuria

Major symptoms

There are symptoms of malaria.

Coffee-colored urine - amniotic fluid, Meyer (+) (with hemoglobinuria).

Red blood cells dropped quickly.

Yellow mucosal skin.

There are malaria parasites in the blood, when the hemolysis has occurred, the malaria parasites are only encountered in 1/3 to 1/4 cases.

Secondary symptoms

Patient is restless, struggling, restless, lightheaded, dizzy.

Vomiting, vomiting green bile yellow bile.

Back pain, pain along the spine.

Swollen, painful liver.

Rapid pulse, fluctuating blood pressure, chest tightness, difficulty breathing in some.

Differential diagnosis

Distinguished with

Hematuria: In stones, cancer, urinary tract tuberculosis, hemorrhagic Dengue ...

Urine has many bile pigments: In viral hepatitis, Leptospirosis hemorrhagic jaundice, cholangitis ...

Myoglobin urine: In burnt, severe burns, myositis, myoglobinuria.

In addition, it should be differentiated from some other hemolytic diseases

Sepsis with complications from hemolytic hematuria (hemolytic staphylococcus, anaerobic bacteria).

Poisoning by poisonous snakes.

Hemoglobinuria syndrome due to transfusion of the wrong blood type, due to the use of foods or strong oxidizing drugs can cause red blood cell destruction in the G6PD enzyme deficient body.

Prevention and treatment of hemorrhagic malaria

Preventive measures

Take good measures to prevent malaria.

Quality treatment of malaria patients.

Good management of malaria patients:

Widely disseminated for people to know for the early self-detection of malaria and hemorrhagic malaria

Treatment

Specific treatment

Discontinue the malaria drug the patient is taking while having hemoglobinuria and switch to another drug. It is best to use artesunat or artemisinin derivatives. If the patient has not taken antimalarial drugs already have hemoglobinuria, also use artemisinin and its derivatives.

Management of entity acute renal failure

The amount of infusion / 24 hours must be cautious, calculated by the formula of urine + vomit + feces + sweat + water loss due to high fever and rapid breathing + 500ml. Addition of electrolytes must be on the electrolyte, in general limit water, salt and fruit high in K +. 5 &. During the infusion, it is necessary to monitor central venous blood pressure, hematocrit, neck veins, liver turbidity area and often listen to the pulmonary background ... to prevent acute pulmonary edema.

Treatment of K + poisoning and acidosis adjustment: Supplement Ca + with 10% calcium gluconate or 10% calcium chloride, depending on the case. Infusion of glucose solution 30% + insulin + natribicarbonate (NaHCO3) 7.5%, limiting the catabolism of protit by diets mainly glucose, hypertonic sweetener solution and protein anabolic drugs such as nerobol, durabolin, use vitamins B1, B2, B121, C.

Indications for hemodialysis, or peritoneal dialysis: It is necessary to do early when blood urea is above 35mmol / l, blood creatinine is 200mmol / l, K + 5.5mmol / l or more, alkaline reserve (HCO3) ≤ 16mmol / l

Standard of discharge

No fever, malaria parasites (-).

Minimize, anuria, hemoglobinuria (-).

Lecture on hemoglobinuria

Deposits in the renal tubules (hemoglobin, tubular epithelial cells) can block the renal tubules, preventing urinary excretion.

Define

Hemoglobinuria is a serious malaria disease caused by acute red blood cell breakdown that causes acute anemia, acute renal failure, jaundice-mucosal jaundice and many other disorders. If not treated properly and promptly, it will lead to death.

Mechanism of pathogenesis

The mechanism of rupture of erythrocytes

Because malaria itself is severe

This leads to severe rupture of erythrocytes and hemoglobinuria, also known as "spontaneous" hemorrhagic malaria (without the involvement of malaria drugs). The likelihood mechanism is due to the following factors:

Increased macrophage activity against both parasites and erythrocytes.

Mechanism of attachment of parasitic infected red blood cells to the endothelium of the vessel wall.

The autoimmune mechanism due to the formation of autoantigens from erythrocytes changes the membrane structure, from which autoantibodies appear.

Due to the role of the drug

Many drugs, including the drug malaria, can cause erythropoiesis and are divided into three groups:

The group of drugs that cause complications in everyone: Sulfon, Phenylhydrazine, acetyl phenylhydrazine.

The group of drugs causing complications in people with unsustainable hemoglobin such as sulfamid, 4 amonoquinolein.

The group of drugs causing complications in people lacking the enzyme G.6.PD such as: Quinine ranks first, followed by primaquin, mepacrin, amidopyrin ...

Stemming from the two above mechanisms, hemoglobinuria is now divided into 2 types:

Malaria patients with hemoglobinuria due to the development of malaria itself: This type of hemorrhagic malaria often arises in severe, recurrent malaria cases due to P. falciparum, this type The variable is usually heavy and very heavy.

Malaria patients with haematuria caused by factors of malaria drugs, the leading is quinine: This type of hemorrhagic malaria can occur in all patients with severe and mild malaria, progressing not massively. as intense as the above type.

Mechanism of hemoglobinuria

Malaria more or less has broken red blood cells, but not everyone has hemoglobinuria. When hemolysis there will be hemoglobin in the blood plasma; Normally 1 liter of plasma has enough haptoglobin to fix 1 g of hemoglobin in the blood plasma; this hemoglobin count will be converted to 40mg bilirubin by endothelial reticulocytes in the liver; When mass hemolysis with hemoglobin greater than 1.35 g in 1 liter of plasma, 1g of hemoglobin will be fixed and converted to bile pigment, leaving 0.35g free hemoglobin in the blood The plasma is a small part is fixed by the plasma albumin to methemalbumin and the remaining free hemoglobin will be excreted through the kidneys in the urine; The renal clearance to hemoglobin is: 6 ml of plasma for 1 minute with hemoglobin concentration of 2-3 g / liter of plasma. Thus hemoglobinuria only occurs in malaria patients when the patient has a strong hemolytic process; impaired hepatic endothelial reticular tissue is an advantageous factor because it is unstable and converts hemoglobin into bilirubin; Renal failure will prolong the excretion of hemoglobin in the urine.

Mechanism of acute renal failure

Patients with hemoglobinuria are more susceptible to physical acute renal failure because:

Massive hemolysis with acute anemia and hypoxia causes tubular necrosis and disturbances of tubular absorption; on the other hand, acute anemia causes blood vessel spasm reflexes and hemodynamic disorder with decreased glomerular filtration; Both types of damage to the kidney tubules and glomeruli lead to acute renal failure: Primary, anuria, in which anemia - renal tubular hypoxia is the main.

Deposits in the renal tubules (hemoglobin, tubular epithelial cells) can obstruct the renal tubules, prevent urinary excretion, but this obstruction is only a secondary, secondary, no basic.

In addition, hemoglobinuria in the first 1-2 days may present with acute functional renal failure due to dehydration (due to vomiting, excessive sweating ...).

clinical

Onset

Usually suddenly, the patient has chills, high fever, headache; pain across the back and spine, often vomiting a lot green - yellow or gagging fluid; mucosal skin turns pale green quickly, sometimes jaundice and early eyes; dark brown urine such as coffee or thick water; Patients often struggle, panicking because of acute lack of oxygen.

Includes the following main symptoms:

Fever becomes seized, vomiting, back pain.

Hemolytic jaundice.

Hemoglobinuria.

Acute anemia and hypoxia.

The patient continued to have a high fever accompanied by chills. Each chills and fever are often accompanied by a haemolytic episode. Continued vomiting of yellow-green stomach fluids and bile. Sweating a lot. Rapid dehydration and electrolyte disturbances.

Jaundice and mucous membranes appear from the end of day one. After each fever and malaria, the yellow color increases again, becoming dark yellow. There are also cases of unknown jaundice (when the hemolysis is mild or the patient's skin is brown).

Hemoglobin urine: At first often reddish brown, later turning black like condensed coffee or thick water because oxyhemoglobin converts to methemoglobin.

Anemia, acute hypoxia: Due to acute and massive hemolysis, the patient has symptoms of acute hypoxia such as pale green mucous skin, or dizziness, dizziness, dizziness, rapid pulse, knife blood pressure moving, shortness of breath, sometimes chest tightness, restlessness, always anxious on the bed, struggling, panic.

Test

Plasmodium

Before hemolysis, malaria parasites can be seen in 75% of cases, but after the episode, only 1 / 4-1 / 3 cases, because many parasitic erythrocytes were broken.

Blood

Fast and severe anemia, in the first day the red blood cells may drop to 1-2 million / mm3 or less, the hemoglobin also decreased. After the haemolysis is over, the blood quickly recovers with signs of regeneration such as: Appearance of young erythrocytes, with alkaline dots, reticulocytes increased. In the case of dehydration, shock, and aneurysms can cause her blood, hemoglobin and red blood cells to artificially increase. The leukocytes usually increase, averaging about 15,000 / mm3, sometimes up to 40-50,000 / mm3 or more, the formula turns left clearly.

Urine

Proteinuria is usually 4 -5 g / l; Urea and Cl- urinary decrease due to tubular failure; has many erythrocyte pigments such as oxyhemoglobin especially methemoglobin and bile pigment like urobilin.

Other tests

Indirect increase in bilirubin in the blood; serum iron increased to 200-300g%; blood urea is always 16 - 80 mmol / liter high, usually very high in the presence of acute renal failure; Potassium is usually high with low urination and physical acute renal failure. Usually there is acidosis with low pH, low alkaline reserve of about 40-30mmol / liter. SGOT and SGPT enzymes are high in some severe cases, when both direct and indirect bilirubin is high.

Developments

The case goes well

The fever goes away quickly, the hemolysis is only 1-2 times and then goes away, the urine fades, returns to normal from day 6 to day 10, red blood cell pigment (hemoglobin) and bile pigment (bilirubin, urobilin) gradually decreased, jaundice gradually faded in parallel with decreased blood bilirubin, erythrocytes increased, blood urea also gradually returned to normal. Recovery takes about 1 month.

The case goes bad

 The fever continued every day with chills, hemolytic episodes recurred every day at the time of the fever, jaundice increased, red blood cells decreased, urine continued to dark brown, the number gradually decreased. 200-400 ml to 40-50ml in 24 hours, even on days of complete anuria, urea increased, the patient turns into acute renal failure, increased blood K +, metabolic acidosis appears, awake the patient, overcast, even in a coma. There are also cases of patients with acute circulatory failure or acute liver failure, or transitioning to an acute encephalopathy due to cerebral hypoxia.

Complications, prognosis, death

Symptoms

Acute renal failure

The most common and dangerous complication, which can appear early, is usually functional acute renal failure due to water deficiency, with high hematocrit, low urination, but urea, creatinine, and Na + clearance are normal; This type is usually mild. From day 4 onwards, acute renal failure is more likely to be due to tubular necrosis: minimal, anuria about 30-100ml / 24 hours, blood urea increased> 7.3 mmol / l, urea is lower than average Usually (<250mmol / 24 hours), creatinine clearance decreases, K + increases by more than 5mmol / l. The patient gradually turns into metabolic acidosis (Kussmaul breathing, Cheynes Stokes), urea poisoning (bloody stools, small pupils, vomiting, gloominess, coma), hyperkalaemia (bloating, paralysis intestinal, low blood pressure, electrocardiogram with symmetrical spike high T waves, wide QRS, loss of P ...), threatening cardiac arrest.

Cardiovascular, circulatory failure

Low blood pressure and rapid pulse are also a common complication due to hemolysis or dehydration and salt causing acute kidney failure and hyperkalaemia. 

Acute brain syndrome

Due to severe hemolysis causing cerebral hypoxia (8.4%), or due to hyperemia coma (5.6%).

Complications in the liver bile

The SGOT and SGPT enzymes are elevated, and the patient has acute liver failure due to acute hepatic parenchymal necrosis.

Prognosis

Symptoms have prognostic significance

Mental state.

Red blood cell count.  

Malaria and hemolytic again.

Vomiting and sweating a lot.

The amount of urine.

 Classification according to prognosis

Signal

Fit

Heavy

Very heavy

Neuropsychiatric

stability

Flustered, struggling, anxious, panic

Overcast, sunset

Respiratory, circulatory

stability

100 rapid pulse, shortness of breath, fluctuating BP

Pulse 100, small, shortness of breath, rapid, shallow, hypotension

Digestive

No vomiting, little vomiting

Vomiting moderate

Vomiting, loose diarrhoea, bloating, hiccups

Blood

Red blood cells 2T-3T

Erythrocytes 1-2T large interval of erythropoiesis

erythrocytes <1T large erythrocytic distance

Urine

500-1000ml/ 24giờ,

light brown

<500 ml / 24 hours, dark brown

<100ml / 24hours, dark brown

Fever and haemolysis

Fever 38 ° C

Light burning

1-2 episodes of hemolysis

High fever 39-40 ° C Shivering

3-4 hemolysis

High fever 39-40 ° C Shivering for many days, 5 or more hemolytic attacks

Jaundice

Bilirubin blood

Urea of ​​blood

Light

£ 85 mmol / litre

7-17 mmol / liter

Fit

> 85 - 170 mmol / liter

> 17-50 mmol / liter

Dark

> 170 mmol / liter

> 50 mmol / liter

Dead

The direct cause of death is usually

Acute renal failure leads to high blood protein, high blood K +, and cardiac arrest.

Seizure coma due to lack of brain oxygen or high blood protein, breathing failure.

Cardiomyopathy, hypotension due to water-electrolyte disturbance, "hemolytic" shock, or myocardial failure due to lack of oxygen or hyperkalaemia.

Diagnosis of hemoglobinuria

Suspected symptoms

Malaria patient has a moderate fever, suddenly has a high fever, before only a mild cold, suddenly there is shivering cold.

Vomiting a lot of "green honey, yellow honey".

Very pain in the back, pain along the spine, pain in the lower ribs.

Skin pale green mucous very quickly, yellowish in eyes appears.

Ending struggling, struggling in bed, feeling dizzy, flustered and panicking every other day.

Urination feels hot foreskin (in some patients).

When encountering these suspicious signs, it is necessary to immediately observe the urine, check the hemoglobinuria.

Diagnosis of hemoglobinuria

Major symptoms

There are symptoms of malaria.

Coffee-coloured urine - amniotic fluid, Meyer (+) (with hemoglobinuria).

Red blood cells dropped quickly.

Yellow mucosal skin.

There are malaria parasites in the blood when the hemolysis has occurred, the malaria parasites are only encountered in 1/3 to 1/4 cases.

Secondary symptoms

The patient is restless, struggling, restless, lightheaded, dizzy.

Vomiting, vomiting green bile yellow bile.

Back pain, pain along the spine.

Swollen, painful liver.

Rapid pulse, fluctuating blood pressure, chest tightness, difficulty breathing in some.

Differential diagnosis

Distinguished with

Hematuria: In stones, cancer, urinary tract tuberculosis, hemorrhagic Dengue ...

Urine has many bile pigments: In viral hepatitis, Leptospirosis hemorrhagic jaundice, cholangitis ...

Myoglobin urine: In burnt, severe burns, myositis, myoglobinuria.

In addition, it should be differentiated from some other hemolytic diseases

Sepsis with complications from hemolytic hematuria (hemolytic staphylococcus, anaerobic bacteria).

Poisoning by poisonous snakes.

Hemoglobinuria syndrome due to transfusion of the wrong blood type, due to the use of foods or strong oxidizing drugs can cause red blood cell destruction in the G6PD enzyme deficient body.

Prevention and treatment of hemorrhagic malaria

Preventive measures

Take good measures to prevent malaria.

Quality treatment of malaria patients.

Good management of malaria patients:

Widely disseminated for people to know for the early self-detection of malaria and hemorrhagic malaria

Treatment

Specific treatment

Discontinue the malaria drug the patient is taking while having hemoglobinuria and switch to another drug. It is best to use artesunate or artemisinin derivatives. If the patient has not taken antimalarial drugs already have hemoglobinuria, also use artemisinin and its derivatives.

Management of entity acute renal failure

The amount of infusion / 24 hours must be cautious, calculated by the formula of urine + vomit + faeces + sweat + water loss due to high fever and rapid breathing + 500ml. Addition of electrolytes must be on the electrolyte, in general, limit water, salt and fruit high in K +. 5 &. During the infusion, it is necessary to monitor central venous blood pressure, hematocrit, neck veins, liver turbidity area and often listen to the pulmonary background ... to prevent acute pulmonary oedema.

Treatment of K + poisoning and acidosis adjustment: Supplement Ca + with 10% calcium gluconate or 10% calcium chloride, depending on the case. Infusion of glucose solution 30% + insulin + natribicarbonate (NaHCO3) 7.5%, limiting the catabolism of protide by diets mainly glucose, hypertonic sweetener solution and protein anabolic drugs such as Neurobiol, Durabolin, use vitamins B1, B2, B121, C.

Indications for hemodialysis, or peritoneal dialysis: It is necessary to do early when blood urea is above 35mmol / l, blood creatinine is 200mmol / l, K + 5.5mmol / l or more, alkaline reserve (HCO3) ≤ 16mmol / l

Standard of discharge

No fever, malaria parasites (-).

Minimize, anuria, hemoglobinuria (-).

Renal function recovery.

Red blood cells > 3 million / mm3 or more.